Journal articles: 'Human Immunodeficient Virus'

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Chalifoux, Laura V., Angela Carville, Douglas Pauley, Brendon Thompson, Andrew A. Lackner, and Keith G. Mansfield. "Enterocytozoon bieneusi as a Cause of Proliferative Serositis in Simian Immunodeficiency Virus–Infected Immunodeficient Macaques (Macaca mulatta)." Archives of Pathology & Laboratory Medicine 124, no. 10 (October 1, 2000): 1480–84. http://dx.doi.org/10.5858/2000-124-1480-ebaaco.

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Abstract Context.—Enterocytozoon bieneusi is the most frequent microsporidian parasite of human patients with acquired immunodeficiency syndrome and is a significant cause of diarrhea and wasting. Recently, this organism has also been recognized as a spontaneous infection of several species of captive macaques. As in humans, E bieneusi frequently causes enteropathy and cholangiohepatitis in immunodeficient simian immunodeficiency virus (SIV)–infected macaques. Objective.—To examine E bieneusi as an etiologic agent of nonsuppurative proliferative serositis in immunodeficient rhesus macaques (Macaca mulatta). Design.—Retrospective analysis of necropsy material obtained from immunodeficient SIV-infected rhesus macaques. Results.—Examination of SIV-infected rhesus macaques (n = 225) revealed E bieneusi proliferative serositis in 7 of 16 cases of peritonitis of unknown origin. The organism could be identified by in situ hybridization and polymerase chain reaction in sections of pleura and peritoneum obtained at necropsy. Serositis was always accompanied by moderate-to-severe infection of the alimentary tract, and morphologic evidence suggested dissemination through efferent lymphatics. Colabeling experiments revealed most infected cells to be cytokeratin positive and less frequently positive for the macrophage marker CD68. Sequencing of a 607–base pair segment of the small subunit ribosomal gene revealed 100% identity to sequences obtained from rhesus macaques (Genbank accession AF023245) and human patients (Genbank accession AF024657 and L16868). Conclusions.—These findings indicate that E bieneusi disseminates in immunodeficient macaques and may be a cause of peritonitis in the immunocompromised host.

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Marusic, Carla, Paola Rizza, Laura Lattanzi, Camillo Mancini, Massimo Spada, Filippo Belardelli, Eugenio Benvenuto, and Imerio Capone. "Chimeric Plant Virus Particles as Immunogens for Inducing Murine and Human Immune Responses against Human Immunodeficiency Virus Type 1." Journal of Virology 75, no. 18 (September 15, 2001): 8434–39. http://dx.doi.org/10.1128/jvi.75.18.8434-8439.2001.

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ABSTRACT The high-yield expression of a neutralizing epitope from human immunodeficiency virus type 1 (HIV-1) on the surface of a plant virus and its immunogenicity are presented. The highly conserved ELDKWA epitope from glycoprotein (gp) 41 was expressed as an N-terminal translational fusion with the potato virus X (PVX) coat protein. The resulting chimeric virus particles (CVPs), purified and used to immunize mice intraperitoneally or intranasally, were able to elicit high levels of HIV-1-specific immunoglobulin G (IgG) and IgA antibodies. Furthermore, the human immune response to CVPs was studied with severe combined immunodeficient mice reconstituted with human peripheral blood lymphocytes (hu-PBL-SCID). hu-PBL-SCID mice immunized with CVP-pulsed autologous dendritic cells were able to mount a specific human primary antibody response against the gp41-derived epitope. Notably, sera from both normal and hu-PBL-SCID mice showed an anti-HIV-1-neutralizing activity. Thus, PVX-based CVPs carrying neutralizing epitopes can offer novel perspectives for the development of effective vaccines against HIV and, more generally, for the design of new vaccination strategies in humans.

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Ito, Yusuke, Kensuke Takaoka, Kazuhiro Toyama, Yoshitaka Wakabayashi, Aya Shinozaki-Ushiku, Aiko Okazaki, Kinuyo Chikamatsu, Satoshi Mitarai, Tetsuo Ushiku, and Mineo Kurokawa. "The First Case of Concomitant Mycobacterium genavense lymphadenitis and EBV-positive lymphoproliferative disorder." Mediterranean Journal of Hematology and Infectious Diseases 12, no. 1 (June 28, 2020): e2020035. http://dx.doi.org/10.4084/mjhid.2020.035.

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This is the first case of concurrent Mycobacterium genavense lymphadenitis and Epstein-Barr virus (EBV)-positive lymphoproliferative disorder (LPD) in the same lymph node with no immunocompromised history. M. genavense infection is a rare opportunistic infection mainly for human immunodeficiency virus (HIV)-infected patients. Although no immunodeficiency was detected in our patient, our case indicates that the immunodeficiency in the background of EBV latency type III and the immunosuppression by malignant lymphoma itself might induce the M. genavense lymphadenitis. This case highly alerts clinicians the immunosuppressive state of EBV-positive LPD with latency type III even if any serological immunodeficient factors are not detected.

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Kim, Jocelyn T., Gabrielle Bresson-Tan, and Jerome A. Zack. "Current Advances in Humanized Mouse Models for Studying NK Cells and HIV Infection." Microorganisms 11, no. 8 (August 2, 2023): 1984. http://dx.doi.org/10.3390/microorganisms11081984.

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Human immunodeficiency virus (HIV) has infected millions of people worldwide and continues to be a major global health problem. Scientists required a small animal model to study HIV pathogenesis and immune responses. To this end, humanized mice were created by transplanting human cells and/or tissues into immunodeficient mice to reconstitute a human immune system. Thus, humanized mice have become a critical animal model for HIV researchers, but with some limitations. Current conventional humanized mice are prone to death by graft versus host disease induced by the mouse signal regulatory protein α and CD47 signaling pathway. In addition, commonly used humanized mice generate low levels of human cytokines required for robust myeloid and natural killer cell development and function. Here, we describe recent advances in humanization procedures and transgenic and knock-in immunodeficient mice to address these limitations.

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Delgado, Sandra, and Jaime Caceres. "Malignant Syphilis in a Human Immunodeficient Virus-Infected Patient." American Journal of Tropical Medicine and Hygiene 96, no. 3 (March 8, 2017): 523–24. http://dx.doi.org/10.4269/ajtmh.16-0755.

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Kumar, Shimareet, Mariarita Santi, Gilbert Vezina, Tena Rosser, Roma S. Chandra, and Robert Keating. "Epstein-Barr Virus-Associated Smooth Muscle Tumor of the Basal Ganglia in an HIV+ Child: Case Report and Review of the Literature." Pediatric and Developmental Pathology 7, no. 2 (March 2004): 198–203. http://dx.doi.org/10.1007/s10024-003-7079-2.

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We describe the clinicopathologic features of an Epstein-Barr virus (EBV)-associated smooth muscle tumor arising in the basal ganglia of a 10-year-old human immunodeficiency virus (HIV)-positive child. Only a few cases of intracranial smooth muscle tumors are reported in the literature and virtually all of these have been extra-axial, involving the dura or sinuses in HIV+ adults. Our case underscores the need to include an EBV-associated smooth muscle tumor in the differential diagnosis when evaluating intracranial mass lesions in immunodeficient children.

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Burns, S. "Podiatric manifestations of AIDS." Journal of the American Podiatric Medical Association 80, no. 1 (January 1, 1990): 15–20. http://dx.doi.org/10.7547/87507315-80-1-15.

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Dermatologic, vascular, neurologic, and musculoskeletal complications are common among persons with acquired immunodeficiency syndrome (AIDS). These manifestations frequently involve the lower extremities and may be the initial presenting symptoms of human immunodeficiency virus (HIV) infection. It is important that practitioners of podiatric medicine be aware of these syndromes to facilitate early diagnosis of AIDS and to provide the best possible care for immunodeficient patients. The author provides a review of the manifestations of AIDS frequently encountered in podiatric practice, along with guidelines for treatment.

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Koka, Prasad S., John K. Fraser, Yvonne Bryson, Gregory C. Bristol, Grace M. Aldrovandi, Eric S. Daar, and Jerome A. Zack. "Human Immunodeficiency Virus Inhibits Multilineage Hematopoiesis In Vivo." Journal of Virology 72, no. 6 (June 1, 1998): 5121–27. http://dx.doi.org/10.1128/jvi.72.6.5121-5127.1998.

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ABSTRACT Human immunodeficiency virus type 1 (HIV-1)-infected individuals often exhibit multiple hematopoietic abnormalities reaching far beyond loss of CD4+ lymphocytes. We used the SCID-hu (Thy/Liv) mouse (severe combined immunodeficient mouse transplanted with human fetal thymus and liver tissues), which provides an in vivo system whereby human pluripotent hematopoietic progenitor cells can be maintained and undergo T-lymphoid differentiation and wherein HIV-1 infection causes severe depletion of CD4-bearing human thymocytes. Herein we show that HIV-1 infection rapidly and severely decreases the ex vivo recovery of human progenitor cells capable of differentiation into both erythroid and myeloid lineages. However, the total CD34+ cell population is not depleted. Combination antiretroviral therapy administered well after loss of multilineage progenitor activity reverses this inhibitory effect, establishing a causal role of viral replication. Taken together, our results suggest that pluripotent stem cells are not killed by HIV-1; rather, a later stage important in both myeloid and erythroid differentiation is affected. In addition, a primary virus isolated from a patient exhibiting multiple hematopoietic abnormalities preferentially depleted myeloid and erythroid colony-forming activity rather than CD4-bearing thymocytes in this system. Thus, HIV-1 infection perturbs multiple hematopoietic lineages in vivo, which may explain the many hematopoietic defects found in infected patients.

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Feichtinger, H., S. L. Li, E. Kaaya, P. Putkonen, K. Grünewald, K. Weyrer, D. Böttiger, I. Ernberg, A. Linde, and G. Biberfeld. "A monkey model for Epstein Barr virus-associated lymphomagenesis in human acquired immunodeficiency syndrome." Journal of Experimental Medicine 176, no. 1 (July 1, 1992): 281–86. http://dx.doi.org/10.1084/jem.176.1.281.

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High-grade malignant nonHodgkin's lymphomas--five lymphoblastic, three pleomorphic, and two immunoblastic--developed in 10/25 cynomolgus monkeys (Macaca fascicularis) followed for up to 746 d after infection with simian immunodeficiency virus, strain SIVsm. These lymphomas were shown to be associated with an Epstein-Barr (EB)-like cynomolgus B-lymphotropic herpesvirus (CBLV) by electron microscopy, by Southern blot hybridization with probes against human EBV, and by the expression of antigens corresponding to EBV-associated nuclear antigens (EBNAs) involved in human B cells transformation. Southern blot demonstration of immunoglobulin gene rearrangements and homogeneous EBV episomes indicated that all the lymphomas were CBLV-associated monoclonal B cell proliferations. Our findings suggest that these tumors correspond to the EBV-associated malignant lymphomas in acquired immunodeficiency syndrome with respect to clinical, morphological, phenotypic, and genotypic characteristics. The particular susceptibility of SIVsm immunodeficient cynomolgus monkeys for CBLV-associated lymphomagenesis appears therefore a useful model for EBV-associated lymphomas in humans.

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Dekate, Jyoti, and Runjan Chetty. "Epstein-Barr Virus–Associated Smooth Muscle Tumor." Archives of Pathology & Laboratory Medicine 140, no. 7 (July 1, 2016): 718–22. http://dx.doi.org/10.5858/arpa.2015-0120-rs.

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Immunodeficient individuals are prone to develop a number of opportunistic infections and unique neoplasms. Epstein-Barr virus–associated smooth muscle tumor is an uncommon neoplasm associated with immunodeficiency. It has been described in patients infected with human immunodeficiency virus, in the posttransplant setting, and in those with congenital immunodeficiency. Different anatomic sites can be involved by Epstein-Barr virus–associated smooth muscle tumor, and even multiple locations can contain these unique lesions within the same patient. The presence of variable numbers of intratumoral lymphocytes and primitive round cell areas are the unique defining features for this tumor. Histopathologic features may vary considerably in terms of cellular atypia, mitotic activity, and necrosis, with no correlation to the clinical behavior. Demonstration of Epstein-Barr virus infection by in situ hybridization within tumor cell remains critical for the diagnosis. The mechanism for Epstein-Barr virus infection of progenitor cells and neoplastic transformation has been an area of interest and conjecture. Different treatment strategies are proposed according to underlying disease status. This paper reviews the clinicopathologic features of this uncommon neoplasm with detailed discussion of the role of Epstein-Barr virus in the pathogenesis.

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Mercader, Maria, Brian J. Nickoloff, and Kimberly E. Foreman. "Induction of Human Immunodeficiency Virus 1 Replication by Human Herpesvirus 8." Archives of Pathology & Laboratory Medicine 125, no. 6 (June 1, 2001): 785–89. http://dx.doi.org/10.5858/2001-125-0785-iohivr.

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Abstract Background.—Human immunodeficiency virus 1 (HIV-1)–infected individuals are commonly infected with herpesviruses, including cytomegalovirus, herpes simplex virus, varicella-zoster virus, and human herpesvirus 8 (HHV-8, also known as Kaposi sarcoma–associated herpesvirus [KSHV]). Previous studies have demonstrated that coinfection with herpesviruses can modulate HIV-1 replication. This can occur either through direct interaction between the 2 viruses or through secondary effects resulting from the release of cellular factors in response to infection. Objective.—To investigate HIV-1 replication in the presence and absence of HHV-8. Design and Methods.—HIV-1 replication was analyzed following culture of HIV-1–infected CD4+ T cells in the presence of HHV-8 infected B-cell lines or control, uninfected B-cell lines. To confirm and extend the results of these in vitro studies, HIV-1–infected T cells were injected into human skin transplanted onto severe combined immunodeficient mice. The human skin was also injected with purified HHV-8 or phosphate-buffered saline as a control and HIV replication measured in biopsy specimens taken 5 to 8 days later. Results and Conclusions.—The results demonstrated a significant increase in HIV-1 replication in the presence of HHV-8 in both the in vitro and in vivo model systems. Although the mechanism responsible for HHV-8 induction of HIV-1 replication remains to be identified, the results indicate that these 2 viruses may interact at the molecular level in coinfected patients, resulting in increased HIV-1 viral load.

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REINHARDT, BARBARA, BRUCE E. TORBETT, RICHARD J. GULIZIA, PETER P. REINHARDT, STEPHEN A. SPECTOR, and DONALD E. MOSIER. "Human Immunodeficiency Virus Type 1 Infection of Neonatal Severe Combined Immunodeficient Mice Xenografted with Human Cord Blood Cells." AIDS Research and Human Retroviruses 10, no. 2 (February 1994): 131–41. http://dx.doi.org/10.1089/aid.1994.10.131.

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Farah, C. S., S. Elahi, K. Drysdale, G. Pang, T. Gotjamanos, G. J. Seymour, R. L. Clancy, and R. B. Ashman. "Primary Role for CD4+ T Lymphocytes in Recovery from Oropharyngeal Candidiasis." Infection and Immunity 70, no. 2 (February 2002): 724–31. http://dx.doi.org/10.1128/iai.70.2.724-731.2002.

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ABSTRACT Oropharyngeal candidiasis is associated with defects in cell-mediated immunity and is commonly seen in human immunodeficiency virus positive individuals and AIDS patients. A model for oral candidiasis in T-cell-deficient BALB/c and CBA/CaH nu/nu mice was established. After inoculation with 108 Candida albicans yeasts, these mice displayed increased levels of oral colonization compared to euthymic control mice and developed a chronic oropharyngeal infection. Histopathological examination of nu/nu oral tissues revealed extensive hyphae penetrating the epithelium, with polymorphonuclear leukocyte microabscess formation. Adoptive transfer of either naive or immune lymphocytes into immunodeficient mice resulted in the recovery of these animals from the oral infection. Reconstitution of immunodeficient mice with naive CD4+ but not CD8+ T cells significantly decreased oral colonization compared to controls. Interleukin-12 and gamma interferon were detected in the draining lymph nodes of immunodeficient mice following reconstitution with naive lymphocytes. This study demonstrates the direct requirement for T lymphocytes in recovery from oral candidiasis and suggests that this is associated with the production of cytokines by CD4+ T helper cells.

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Wesołowski, Roland, Marta Pawłowska, Małgorzata Smoguła, and Karolina Szewczyk-Golec. "Advances and Challenges in Diagnostics of Toxoplasmosis in HIV-Infected Patients." Pathogens 12, no. 1 (January 9, 2023): 110. http://dx.doi.org/10.3390/pathogens12010110.

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Toxoplasma gondii is a worldwide distributed protozoan parasite. This apicomplexan parasite infects one-third of the population worldwide, causing toxoplasmosis, considered one of the neglected parasitic infections. In healthy humans, most infections are asymptomatic. However, in immunocompromised patients, the course of the disease can be life-threatening. Human immunodeficiency virus (HIV)-infected patients have a very high burden of Toxoplasma gondii co-infection. Thus, it is essential to use modern, sensitive, and specific methods to properly monitor the course of toxoplasmosis in immunodeficient patients.

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Uckun, Fatih M., Lisa M. Chelstrom, Lisa Tuel-Ahlgren, Ilker Dibirdik, James D. Irvin, Mridula-Chandan Langlie, and Dorothea E. Myers. "TXU (Anti-CD7)-Pokeweed Antiviral Protein as a Potent Inhibitor of Human Immunodeficiency Virus." Antimicrobial Agents and Chemotherapy 42, no. 2 (February 1, 1998): 383–88. http://dx.doi.org/10.1128/aac.42.2.383.

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ABSTRACT We have evaluated the clinical potential of TXU (anti-CD7)-pokeweed antiviral protein (PAP) immunoconjugate (TXU-PAP) as a new biotherapeutic anti-human immunodeficiency virus (anti-HIV) agent by evaluating its anti-HIV type 1 (anti-HIV-1) activity in vitro, as well as in a surrogate human peripheral blood lymphocyte-severe combined immunodeficient (Hu-PBL-SCID) mouse model of human AIDS. The present report documents in a side-by-side comparison the superior in vitro anti-HIV-1 activity of TXU-PAP compared to the activities of zidovudine, 2′,3′-didehydro-2′,3′-dideoxythymidine, unconjugated PAP, and B53-PAP, an anti-CD4-PAP immunoconjugate. Notably, TXU-PAP elicited potent anti-HIV activity in the Hu-PBL-SCID mouse model of human AIDS without any side effects and at doses that were very well tolerated by cynomolgus monkeys. Furthermore, plasma samples from TXU-PAP-treated cynomolgus monkeys showed potent anti-HIV-1 activity in vitro.

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Griffin, William C., Lawrence D. Middaugh, Jennifer E. Cook, and William R. Tyor. "The severe combined immunodeficient (SCID) mouse model of human immunodeficiency virus encephalitis: Deficits in cognitive function." Journal of Neurovirology 10, no. 2 (January 2004): 109–15. http://dx.doi.org/10.1080/13550280490428333.

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Silva, Dorotéa Lobato da, Renato Lopes Fernandes de Medeiros, Marluce Matos de Moraes, and Fernanda Sagicado Espírito Santo. "Restriction enzyme analysis of the human cytomegalovirus genome in specimens collected from immunodeficient patients in Belém, State of Pará, Brazil." Revista da Sociedade Brasileira de Medicina Tropical 44, no. 5 (August 19, 2011): 551–54. http://dx.doi.org/10.1590/s0037-86822011005000052.

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INTRODUCTION: Human cytomegalovirus is an opportunistic betaherpesvirus that causes persistent and serious infections in immunodeficient patients. Recurrent infections occur due to the presence of the virus in a latent state in some cell types. It is possible to examine the virus using molecular methods to aid in the immunological diagnosis and to generate a molecular viral profile in immunodeficient patients. The objective of this study was to characterize cytomegalovirus genotypes and to generate the epidemiological and molecular viral profile in immunodeficient patients. METHODS: A total of 105 samples were collected from immunodeficient patients from the City of Belém, including newborns, hemodialysis patients, transplant recipients and HIV+ patients. An IgG and IgM antibody study was completed using ELISA, and enzymatic analysis by restriction fragment length polymorphism (RFLP) was performed to characterize viral genotypes. RESULTS: It was observed that 100% of the patients had IgG antibodies, 87% of which were IgG+/IgM-, consistent with a prior infection profile, 13% were IgG+/IgM+, suggestive of recent infection. The newborn group had the highest frequency (27%) of the IgG+/IgM+ profile. By RFLP analysis, only one genotype was observed, gB2, which corresponded to the standard AD169 strain. CONCLUSIONS: The presence of IgM antibodies in new borns indicates that HCMV continues to be an important cause of congenital infection. The low observed genotypic diversity could be attributed to the small sample size because newborns were excluded from the RFLP analysis. This study will be continued including samples from newborns to extend the knowledge of the general and molecular epidemiology of HCMV in immunodeficient patients.

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Sánchez‐Velasco, Pablo, Javier G. Ocejo‐Vinyals, Reyes Flores, José J. Gómez‐Román, María‐José Lozano, and Francisco Leyva‐Cobián. "Simultaneous Multiorgan Presence of Human Herpesvirus 8 and Restricted Lymphotropism of Epstein‐Barr Virus DNA Sequences in a Human Immunodeficiency Virus–Negative Immunodeficient Infant." Journal of Infectious Diseases 183, no. 2 (January 15, 2001): 338–42. http://dx.doi.org/10.1086/317925.

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Khanna, Nina, Marcel Wolbers, Nicolas J. Mueller, Christian Garzoni, Renaud A. Du Pasquier, Christoph A. Fux, Pietro Vernazza, et al. "JC Virus-Specific Immune Responses in Human Immunodeficiency Virus Type 1 Patients with Progressive Multifocal Leukoencephalopathy." Journal of Virology 83, no. 9 (February 11, 2009): 4404–11. http://dx.doi.org/10.1128/jvi.02657-08.

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ABSTRACT Progressive multifocal leukoencephalopathy (PML) is a frequently fatal disease caused by uncontrolled polyomavirus JC (JCV) in severely immunodeficient patients. We investigated the JCV-specific cellular and humoral immunity in the Swiss HIV Cohort Study. We identified PML cases (n = 29), as well as three matched controls per case (n = 87), with prospectively cryopreserved peripheral blood mononuclear cells and plasma at diagnosis. Nested controls were matched according to age, gender, CD4+ T-cell count, and decline. Survivors (n = 18) were defined as being alive for >1 year after diagnosis. Using gamma interferon enzyme-linked immunospot assays, we found that JCV-specific T-cell responses were lower in nonsurvivors than in their matched controls (P = 0.08), which was highly significant for laboratory- and histologically confirmed PML cases (P = 0.004). No difference was found between PML survivors and controls or for cytomegalovirus-specific T-cell responses. PML survivors showed significant increases in JCV-specific T cells (P = 0.04) and immunoglobulin G (IgG) responses (P = 0.005). IgG responses in survivors were positively correlated with CD4+ T-cell counts (P = 0.049) and negatively with human immunodeficiency virus RNA loads (P = 0.03). We conclude that PML nonsurvivors had selectively impaired JCV-specific T-cell responses compared to CD4+ T-cell-matched controls and failed to mount JCV-specific antibody responses. JCV-specific T-cell and IgG responses may serve as prognostic markers for patients at risk.

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Weiss, Robin A. "The Leeuwenhoek Lecture 2001. Animal origins of human infectious disease." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 356, no. 1410 (June 29, 2001): 957–77. http://dx.doi.org/10.1098/rstb.2001.0838.

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Since time immemorial animals have been a major source of human infectious disease. Certain infections like rabies are recognized as zoonoses caused in each case by direct animal–to–human transmission. Others like measles became independently sustained with the human population so that the causative virus has diverged from its animal progenitor. Recent examples of direct zoonoses are variant Creutzfeldt–Jakob disease arising from bovine spongiform encephalopathy, and the H5N1 avian influenza outbreak in Hong Kong. Epidemics of recent animal origin are the 1918–1919 influenza pandemic, and acquired immune deficiency syndrome caused by human immunodeficiency virus (HIV). Some retroviruses jump into and out of the chromosomal DNA of the host germline, so that they oscillate between being inherited Mendelian traits or infectious agents in different species. Will new procedures like animal–to–human transplants unleash further infections? Do microbes become more virulent upon cross–species transfer? Are animal microbes a threat as biological weapons? Will the vast reservoir of immunodeficient hosts due to the HIV pandemic provide conditions permissive for sporadic zoonoses to take off as human–tohuman transmissible diseases? Do human infections now pose a threat to endangered primates? These questions are addressed in this lecture.

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Eddy Warman, Nur ‘Aini, and Nurul Yaqeen Mohd Esa. "A Rare and Challenging Case of Pulmonary Mycobacterium genavense in an Immunocompetent Adult." Journal of Clinical and Health Sciences 3, no. 1 (June 30, 2018): 47. http://dx.doi.org/10.24191/jchs.v3i1.6158.

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Mycobacterium genavense, a non-tuberculous mycobacterium (NTM), usually affects patients severely immunodeficient from human immunodeficiency virus (HIV) infection or any other immunocompromised states. We reported a case in a 70-year-old female with well-controlled diabetes and history of proximal cystic bronchiectasis. She presented with 2 months history of cough, haemoptysis, and night sweats of which serial sputa were positive for acid-fast bacilli and the culture repeatedly grew M. genavense. Treatment with rifampicin, ofloxacin, and clarithromycin was complicated with drug-induced liver injury and intractable gastrointestinal side effects. We also presented a brief review of relevant literature.

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Koka, Prasad S., Beth D. Jamieson, David G. Brooks, and Jerome A. Zack. "Human Immunodeficiency Virus Type 1-Induced Hematopoietic Inhibition Is Independent of Productive Infection of Progenitor Cells In Vivo." Journal of Virology 73, no. 11 (November 1, 1999): 9089–97. http://dx.doi.org/10.1128/jvi.73.11.9089-9097.1999.

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ABSTRACT Human immunodeficiency virus (HIV)-infected individuals exhibit a variety of hematopoietic dysfunctions. The SCID-hu mouse (severe combined immunodeficient mouse transplanted with human fetal thymus and liver tissues) can be used to model the loss of human hematopoietic precursor cell function following HIV infection and has a distinct advantage in that data can be obtained in the absence of confounding factors often seen in infected humans. In this study, we establish that HIV type 1 (HIV-1) bearing a reporter gene inserted into the viralvpr gene is highly aggressive in depleting human myeloid and erythroid colony-forming precursor activity in vivo. Human CD34+ progenitor cells can be efficiently recovered from infected implants yet do not express the viral reporter gene, despite severe functional defects. Our results indicate that HIV-1 infection alone leads to hematopoietic inhibition in vivo; however, this effect is due to indirect mechanisms rather than to direct infection of CD34+ cells in vivo.

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Brown, Scott A., Julia L. Hurwitz, Amy Zirkel, Sherri Surman, Toru Takimoto, Irina Alymova, Chris Coleclough, Allen Portner, Peter C. Doherty, and Karen S. Slobod. "A Recombinant Sendai Virus Is Controlled by CD4+ Effector T Cells Responding to a Secreted Human Immunodeficiency Virus Type 1 Envelope Glycoprotein." Journal of Virology 81, no. 22 (July 25, 2007): 12535–42. http://dx.doi.org/10.1128/jvi.00197-07.

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ABSTRACT The importance of antigen-specific CD4+ helper T cells in virus infections is well recognized, but their possible role as direct mediators of virus clearance is less well characterized. Here we describe a recombinant Sendai virus strategy for probing the effector role(s) of CD4+ T cells. Mice were vaccinated with DNA and vaccinia virus recombinant vectors encoding a secreted human immunodeficiency virus type 1 (HIV-1) envelope protein and then challenged with a Sendai virus carrying a homologous HIV-1 envelope gene. The primed mice showed (i) prompt homing of numerous envelope-primed CD4+ T cell populations to the virus-infected lung, (ii) substantial production of gamma interferon, and interleukin-2 (IL-2), IL-4, and IL-5 in that site, and (iii) significantly reduced pulmonary viral load. The challenge experiments were repeated with immunoglobulin−/− μMT mice in the presence or absence of CD8+ and/or CD4+ T cells. These selectively immunodeficient mice were protected by primed CD4+ T cells in the absence of antibody or CD8+ T cells. Together, these results highlight the role of CD4+ T cells as direct effectors in vivo and, because this protocol gives such a potent response, identify an outstanding experimental model for further dissecting CD4+ T-cell-mediated immunity in the lung.

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Gorantla, Santhi, Kathlyn Santos, VaKara Meyer, Stephen Dewhurst, William J. Bowers, Howard J. Federoff, Howard E. Gendelman, and Larisa Poluektova. "Human Dendritic Cells Transduced with Herpes Simplex Virus Amplicons Encoding Human Immunodeficiency Virus Type 1 (HIV-1) gp120 Elicit Adaptive Immune Responses from Human Cells Engrafted into NOD/SCID Mice and Confer Partial Protection against HIV-1 Challenge." Journal of Virology 79, no. 4 (February 15, 2005): 2124–32. http://dx.doi.org/10.1128/jvi.79.4.2124-2132.2005.

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ABSTRACT Small-animal models are needed to test human immunodeficiency virus (HIV) vaccine efficacy following viral challenge. To this end, we examined HIV-1-specific immune responses following immunization of nonobese diabetic-severe combined immunodeficient mice that were repopulated with human peripheral blood lymphocytes (hu-PBL-NOD/SCID mice). Autologous dendritic cells (DC) were transduced ex vivo with replication-defective, helper virus-free, herpes simplex virus type 1 (HSV-1) amplicons that expressed HIV-1 gp120 and were then injected into the hu-PBL-NOD/SCID mice. This resulted in primary HIV-1-specific humoral and cellular immune responses. Serum samples from vaccinated animals contained human immunoglobulin G that reacted with HIV-1 Env proteins by enzyme-linked immunosorbent assay and neutralized the infectivity of HIV-1 LAI and ADA strains. T cells isolated from the mice responded to viral antigens by producing gamma interferon when analyzed by enzyme-linked immunospot assay. Importantly, exposure of the vaccinated animals to infectious HIV-1 demonstrated partial protection against infectious HIV-1 challenge. This was reflected by a reduction in HIV-1ADA and by protection of the engrafted human CD4+ T lymphocytes against HIV-1LAI-induced cytotoxicity. These data demonstrate that transduction of DC by HSV amplicon vectors expressing HIV-1 gp120 induce virus-specific immune responses in hu-PBL-NOD/SCID mice. This mouse model may be a useful tool to evaluate human immune responses and protection against viral infection following vaccination.

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Roth, Michael D., Donald P. Tashkin, Ruth Choi, Beth D. Jamieson, Jerome A. Zack, and Gayle Cocita Baldwin. "Cocaine Enhances Human Immunodeficiency Virus Replication in a Model of Severe Combined Immunodeficient Mice Implanted with Human Peripheral Blood Leukocytes." Journal of Infectious Diseases 185, no. 5 (March 2002): 701–5. http://dx.doi.org/10.1086/339012.

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Bateman, Caroline M., Alison Kesson, Madeleine Powys, Melanie Wong, and Emily Blyth. "Cytomegalovirus Infections in Children with Primary and Secondary Immune Deficiencies." Viruses 13, no. 10 (October 5, 2021): 2001. http://dx.doi.org/10.3390/v13102001.

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Cytomegalovirus (CMV) is a human herpes virus that causes significant morbidity and mortality in immunosuppressed children. CMV primary infection causes a clinically mild disease in healthy children, usually in early childhood; the virus then utilises several mechanisms to establish host latency, which allows for periodic reactivation, particularly when the host is immunocompromised. It is this reactivation that is responsible for the significant morbidity and mortality in immunocompromised children. We review CMV infection in the primary immunodeficient host, including early identification of these infants by newborn screening to allow for CMV infection prevention strategies. Furthermore, clinical CMV is discussed in the context of children treated with secondary immunodeficiency, particularly paediatric cancer patients and children undergoing haematopoietic stem cell transplant (HSCT). Treatments for CMV are highlighted and include CMV immunotherapy.

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27

Hege, Kristen M., Keegan S. Cooke, Mitchell H. Finer, Krisztina M. Zsebo, and Margo R. Roberts. "Systemic T Cell–independent Tumor Immunity after Transplantation of Universal Receptor–modified Bone Marrow into SCID Mice." Journal of Experimental Medicine 184, no. 6 (December 1, 1996): 2261–70. http://dx.doi.org/10.1084/jem.184.6.2261.

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Gene modification of hematopoietic stem cells (HSC) with antigen-specific, chimeric, or “universal” immune receptors (URs) is a novel but untested form of targeted immunotherapy. A human immunodeficiency virus (HIV) envelope–specific UR consisting of the extracellular domain of human CD4 linked to the ζ chain of the T cell receptor (CD4ζ) was introduced ex vivo into murine HSC by retroviral transduction. After transplantation into immunodeficient SCID mice, sustained high level expression of CD4ζ was observed in circulating myeloid and natural killer cells. CD4ζ-transplanted mice were protected from challenge with a lethal dose of a disseminated human leukemia expressing HIV envelope. These results demonstrate the ability of chimeric receptors bearing ζ-signaling domains to activate non–T cell effector populations in vivo and thereby mediate systemic immunity.

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Navarro, Maritza, and I. Celine Hanson. "ENCEPHALOPATHY IN CHILDREN WITH PERINATALLY ACQUIRED HUMAN IMMUNODEFICIENCY VIRUS INFECTION." Pediatrics 98, no. 2 (August 1, 1996): 344–45. http://dx.doi.org/10.1542/peds.98.2.344a.

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HIV-induced encephalopathy is common among children with vertically acquired HIV (10% of HIV infected children; 23% of children with AIDS). HIV encephalopathy represents 12% of first-reported ADCs and 12% of subsequent ADCs. Most cases were diagnosed by 3 years of age and the highest risk occurred during the first year of life. No demographic or birth characteristics predicted the development of encephalopathy. An association between cardiomyopathy and encephalopathy was noted. Children with HIV encephalopathy were severely immunodeficient, and survival time was poor. This report demonstrates the dramatic clinical effect of HIV infection in producing marked immunosuppression with impact on additional organ systems; ie, central nervous system.

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29

Grote, Deanna, Stephen J. Russell, Tatjana I. Cornu, Roberto Cattaneo, Richard Vile, Gregory A. Poland, and Adele K. Fielding. "Live attenuated measles virus induces regression of human lymphoma xenografts in immunodeficient mice." Blood 97, no. 12 (June 15, 2001): 3746–54. http://dx.doi.org/10.1182/blood.v97.12.3746.

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Derivatives of the Edmonston-B strain of measles virus (MV-Ed) are safe, live attenuated measles virus (MV) vaccines that have been used worldwide for more than 30 years. The cytoreductive potential of MV-Ed has been investigated in murine models of both aggressive and indolent B-cell lymphoma in severe combined immunodeficient (SCID) mice. The rationale for these studies was generated by experience with viral fusogenic membrane glycoproteins as cytotoxic genes and the recognition of the potential of replicating viruses in the treatment of human malignancy. Intratumoral injection of both unmodified MV-Ed and a strain of MV-Ed genetically modified by the addition of a β-galactosidase reporter gene (MVlacZ) induced regression of large established human lymphoma xenografts, in contrast to control therapy with UV-inactivated virus, in which all tumors progressed. The antitumor effect still occurred in the presence of passively transferred anti-MV antibody. Intravenous administration of MV also resulted in considerable slowing of tumor progression. Analysis of sections of residual tumor confirmed replication of MV within the tumors. Thus, the vaccine strain of MV mediates regression of large, established human B-cell lymphoma xenografts in SCID mice, and proof of principle is established that MV is oncolytic for lymphomas in vivo. Attenuated MVs may have value as a novel replicating-virus therapy for this group of disorders.

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Segall, H., I. Lubin, H. Marcus, A. Canaan, and Y. Reisner. "Generation of primary antigen-specific human cytotoxic T lymphocytes in human/mouse radiation chimera." Blood 88, no. 2 (July 15, 1996): 721–30. http://dx.doi.org/10.1182/blood.v88.2.721.bloodjournal882721.

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Severe combined immunodeficient (SCID) mice are increasingly used as hosts for the adoptive transfer of human lymphocytes. Human antibody responses can be obtained in these xenogeneic chimeras, but information about the functionality of the human T cells in SCID mice is limited and controversial. Studies using human peripheral blood lymphocytes (PBL) injected intraperitoneally (IP) into SCID mice (hu-PBL-SCID mice) have shown that human T cells from these chimeras are anergic and have a defective signaling via the T-cell receptor. In addition, their antigenic repertoire is limited to xenoreactive clones. In the present study, we tested the functionality of human T cell in a recently described chimeric model. In this system, BALB/c mice are conditioned by irradiation and then transplanted with SCID bone marrow, followed by IP injection of human PBL. Our experiments demonstrated that human T cells, recovered from these hu-PBL-BALB mice within 1 month posttransplant, proliferated and expressed activation markers upon stimulation with anti-CD3 monoclonal antibody. A vigorous antiallogeneic human cytotoxic T-lymphocyte (CTL) response could be generated in these mice by immunizing them with irradiated allogeneic cells. Moreover, anti-human immunodeficiency virus type 1 (HIV-1) Net- specific human CTLs could be generated in vivo from naive lymphocytes by immunization of mouse-human chimeras with a recombinant vaccinia-nef virus. This model may be used to evaluate potential immunomodulatory drugs or cytokines, and could provide a relevant model for testing HIV vaccines, for production of antiviral T-cell clones for adoptive therapy, and for studying human T-cell responses in vivo.

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Kaiser, Marco, Déborah Delaune, Olivier Chazouillères, Johannes Blümel, Anne-Marie Roque-Afonso, and Sally A. Baylis. "A World Health Organization Human Hepatitis E Virus Reference Strain Related to Similar Strains Isolated from Rabbits." Genome Announcements 6, no. 16 (April 19, 2018): e00292-18. http://dx.doi.org/10.1128/genomea.00292-18.

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ABSTRACT We report here the genome sequence of a hepatitis E virus (HEV) strain from a chronically infected immunodeficient patient. Full-length sequence analysis revealed a distinct HEV strain, of a tentative new subgenotype, clustering with viruses from rabbits. It is a World Health Organization reference strain for validation of nucleic acid testing.

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Ober, B. T., P. Brühl, M. Schmidt, V. Wieser, W. Gritschenberger, S. Coulibaly, H. Savidis-Dacho, M. Gerencer, and F. G. Falkner. "Immunogenicity and Safety of Defective Vaccinia Virus Lister: Comparison with Modified Vaccinia Virus Ankara." Journal of Virology 76, no. 15 (August 1, 2002): 7713–23. http://dx.doi.org/10.1128/jvi.76.15.7713-7723.2002.

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ABSTRACT Potent and safe vaccinia virus vectors inducing cell-mediated immunity are needed for clinical use. Replicating vaccinia viruses generally induce strong cell-mediated immunity; however, they may have severe adverse effects. As a vector for clinical use, we assessed the defective vaccinia virus system, in which deletion of an essential gene blocks viral replication, resulting in an infectious virus that does not multiply in the host. The vaccinia virus Lister/Elstree strain, used during worldwide smallpox eradication, was chosen as the parental virus. The immunogenicity and safety of the defective vaccinia virus Lister were evaluated without and with the inserted human p53 gene as a model and compared to parallel constructs based on modified vaccinia virus Ankara (MVA), the present “gold standard” of recombinant vaccinia viruses in clinical development. The defective viruses induced an efficient Th1-type immune response. Antibody and cytotoxic-T-cell responses were comparable to those induced by MVA. Safety of the defective Lister constructs could be demonstrated in vitro in cell culture as well as in vivo in immunodeficient SCID mice. Similar to MVA, the defective viruses were tolerated at doses four orders of magnitude higher than those of the wild-type Lister strain. While current nonreplicating vectors are produced mainly in primary chicken cells, defective vaccinia virus is produced in a permanent safety-tested cell line. Vaccines based on this system have the additional advantage of enhanced product safety. Therefore, a vector system was made which promises to be a valuable tool not only for immunotherapy for diseases such as cancer, human immunodeficiency virus infection, or malaria but also as a basis for a safer smallpox vaccine.

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Pisa, P., MJ Cannon, EK Pisa, NR Cooper, and RI Fox. "Epstein-Barr virus induced lymphoproliferative tumors in severe combined immunodeficient mice are oligoclonal." Blood 79, no. 1 (January 1, 1992): 173–79. http://dx.doi.org/10.1182/blood.v79.1.173.173.

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Abstract Severe combined immunodeficient (SCID) mice reconstituted with lymphocytes from Epstein-Barr virus (EBV) negative human donors develop aggressive tumors after the chimeric mice are infected with EBV. The tumors were composed of human B cells that expressed EBV encoded antigens (latent membrane protein and EBV nuclear antigen2). Southern blot analysis of DNA from 16 SCID/hu tumors with human Ig gene probes showed that each tumor contained multiple heavy and light chain gene rearrangements. Ig kappa gene rearrangements were frequent, while clonal lambda gene rearrangements were infrequent. Analysis of EBV terminal repeat sequences indicated two or more fused termini in each tumor, consistent with a multiclonal origin. Linear terminal repeat segments and viral antigens (EA-D and EA-R) associated with EBV replication were not detected in the tumors. High levels of human Igs in the SCID/hu serum were oligoclonal and primarily contained kappa light chains. Before the appearance of overt tumors, circulating cells with human and EBV DNA could be detected in the SCID/hu mice by the polymerase chain reaction. We conclude that EBV infection in SCID/hu chimeric mice produces a limited number of transformation events, which give rise to oligoclonal tumors resembling EBV-associated lymphoproliferative disorders in some immune-deficient patients.

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Pisa, P., MJ Cannon, EK Pisa, NR Cooper, and RI Fox. "Epstein-Barr virus induced lymphoproliferative tumors in severe combined immunodeficient mice are oligoclonal." Blood 79, no. 1 (January 1, 1992): 173–79. http://dx.doi.org/10.1182/blood.v79.1.173.bloodjournal791173.

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Severe combined immunodeficient (SCID) mice reconstituted with lymphocytes from Epstein-Barr virus (EBV) negative human donors develop aggressive tumors after the chimeric mice are infected with EBV. The tumors were composed of human B cells that expressed EBV encoded antigens (latent membrane protein and EBV nuclear antigen2). Southern blot analysis of DNA from 16 SCID/hu tumors with human Ig gene probes showed that each tumor contained multiple heavy and light chain gene rearrangements. Ig kappa gene rearrangements were frequent, while clonal lambda gene rearrangements were infrequent. Analysis of EBV terminal repeat sequences indicated two or more fused termini in each tumor, consistent with a multiclonal origin. Linear terminal repeat segments and viral antigens (EA-D and EA-R) associated with EBV replication were not detected in the tumors. High levels of human Igs in the SCID/hu serum were oligoclonal and primarily contained kappa light chains. Before the appearance of overt tumors, circulating cells with human and EBV DNA could be detected in the SCID/hu mice by the polymerase chain reaction. We conclude that EBV infection in SCID/hu chimeric mice produces a limited number of transformation events, which give rise to oligoclonal tumors resembling EBV-associated lymphoproliferative disorders in some immune-deficient patients.

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35

Kelly, Patrick F., Jody Vandergriff, Amit Nathwani, Arthur W. Nienhuis, and Elio F. Vanin. "Highly efficient gene transfer into cord blood nonobese diabetic/severe combined immunodeficiency repopulating cells by oncoretroviral vector particles pseudotyped with the feline endogenous retrovirus (RD114) envelope protein." Blood 96, no. 4 (August 15, 2000): 1206–14. http://dx.doi.org/10.1182/blood.v96.4.1206.

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Abstract Limited expression of the amphotropic envelope receptor is a recognized barrier to efficient oncoretroviral vector–mediated gene transfer. Human hematopoietic cell lines and cord blood–derived CD34+ and CD34+, CD38− cell populations and the progenitors contained therein were transduced far more efficiently with oncoretroviral particles pseudotyped with the envelope protein of feline endogenous virus (RD114) than with conventional amphotropic vector particles. Similarly, human repopulating cells from umbilical cord blood capable of establishing hematopoiesis in immunodeficient mice were efficiently transduced with RD114-pseudotyped particles, whereas amphotropic particles were ineffective at introducing the proviral genome. After only a single exposure of CD34+ cord blood cells to RD114-pseudotyped particles, all engrafted nonobese diabetic/severe combined immunodeficiency mice (15 of 15) contained genetically modified human bone marrow cells. Human cells that were positive for enhanced green fluorescent protein represented as much as 90% of the graft. The use of RD114-pseudotyped vectors may be advantageous for therapeutic gene transfer into hematopoietic stem cells.

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36

Kelly, Patrick F., Jody Vandergriff, Amit Nathwani, Arthur W. Nienhuis, and Elio F. Vanin. "Highly efficient gene transfer into cord blood nonobese diabetic/severe combined immunodeficiency repopulating cells by oncoretroviral vector particles pseudotyped with the feline endogenous retrovirus (RD114) envelope protein." Blood 96, no. 4 (August 15, 2000): 1206–14. http://dx.doi.org/10.1182/blood.v96.4.1206.h8001206_1206_1214.

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Limited expression of the amphotropic envelope receptor is a recognized barrier to efficient oncoretroviral vector–mediated gene transfer. Human hematopoietic cell lines and cord blood–derived CD34+ and CD34+, CD38− cell populations and the progenitors contained therein were transduced far more efficiently with oncoretroviral particles pseudotyped with the envelope protein of feline endogenous virus (RD114) than with conventional amphotropic vector particles. Similarly, human repopulating cells from umbilical cord blood capable of establishing hematopoiesis in immunodeficient mice were efficiently transduced with RD114-pseudotyped particles, whereas amphotropic particles were ineffective at introducing the proviral genome. After only a single exposure of CD34+ cord blood cells to RD114-pseudotyped particles, all engrafted nonobese diabetic/severe combined immunodeficiency mice (15 of 15) contained genetically modified human bone marrow cells. Human cells that were positive for enhanced green fluorescent protein represented as much as 90% of the graft. The use of RD114-pseudotyped vectors may be advantageous for therapeutic gene transfer into hematopoietic stem cells.

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37

Pai, Sung-Yun, Kathryn Lurain, and Robert Yarchoan. "How immunodeficiency can lead to malignancy." Hematology 2021, no. 1 (December 10, 2021): 287–95. http://dx.doi.org/10.1182/hematology.2021000261.

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Abstract Immunodeficiency, whether acquired in the case of human immunodeficiency virus (HIV) infection or congenital due to inborn errors of immunity (IEIs), presents clinically with not only infection and immune dysregulation but also increased risk of malignancy. The range of malignancies seen is relatively limited and attributable to the particular cellular and molecular defects in each disease. CD4+ T-cell lymphopenia in people living with HIV infection (PLWH) and certain IEIs drive the predisposition to aggressive B-cell non-Hodgkin lymphomas, including certain rare subtypes rarely seen in immunocompetent individuals. PLWH and IEI that lead to profound T-cell lymphopenia or dysfunction also are at risk of cancers related to oncogenic viruses such as Kaposi sarcoma herpesvirus, Epstein-Barr virus, human papillomavirus (HPV), and Merkel cell polyomavirus. IEIs that affect natural killer cell development and/or function heavily predispose to HPV-associated epithelial cancers. Defects in DNA repair pathways compromise T- and B-lymphocyte development during immune receptor rearrangement in addition to affecting hematopoietic and epithelial DNA damage responses, resulting in both hematologic and nonhematologic cancers. Treatment of cancers in immunodeficient individuals should be curative in intent and pursued in close consultation with disease experts in immunology and infectious disease.

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38

Hartsfield, C. L., D. Lipke, Y. L. Lai, D. A. Cohen, and M. N. Gillespie. "Pulmonary mechanical and immunologic dysfunction in a murine model of AIDS." American Journal of Physiology-Lung Cellular and Molecular Physiology 272, no. 4 (April 1, 1997): L699—L706. http://dx.doi.org/10.1152/ajplung.1997.272.4.l699.

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Human immunodeficiency virus-infected patients occasionally exhibit alveolar septal wall thickening and decreases in gas diffusion capacity, but the mechanism underlying these abnormalities is unknown. The present study evaluated septal wall thickness and gas exchange properties in a murine model of the acquired immunodeficiency syndrome and determined whether there were alterations in lung lymphocyte deposition and activation that could contribute to changes in respiratory structure and function. Although alveolar septal wall thickness did not differ from control at 1, 2, and 4 wk postimmunosuppressive virus infection, at 8 wk after infection, septal wall thickness was substantially increased. Immunohistochemical evaluation at this time revealed marked increases in the septal wall deposition of fibronectin and collagen type IV. Pulmonary function tests on anesthetized mice with virus-induced septal wall thickening demonstrated that, although total lung capacity, compliance, and functional residual capacity were unaltered, diffusion capacity for carbon monoxide was significantly impaired. A diffuse nonspecific interstitial pneumonitis was present in lungs of immunodeficient mice, and flow cytometry indicated that both lymphocytes and macrophages were activated. Reverse transcriptase-polymerase chain reaction analysis of lung lymphocytes demonstrated enhanced mRNA expression for several cytokines known to affect lung structure. These results show that impaired gas exchange occurs in a murine model of acquired immunodeficiency syndrome and suggest that such alterations may be mediated by elaboration of cytokines from activated lung lymphocytes and macrophages.

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Florea, Anca V., Diana N. Ionescu, and Mona F. Melhem. "Parvovirus B19 Infection in the Immunocompromised Host." Archives of Pathology & Laboratory Medicine 131, no. 5 (May 1, 2007): 799–804. http://dx.doi.org/10.5858/2007-131-799-pbiiti.

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Abstract Human parvovirus B19 is a single-stranded DNA virus with a predilection for infecting rapidly dividing cell lines, such as bone marrow erythroid progenitor cells. People with defective cell-mediated immunity (eg, severe combined immunodeficiency syndrome; acquired immunodeficiency syndrome; and patients receiving immunosuppressive therapy, ie, post organ transplant) can develop pure red cell aplasia, in which suppression of erythroid precursors is permanent. Identification of parvovirus inclusions in marrow biopsies and subsequent confirmation of infection by in situ hybridization is important in the assessment of anemia in immunodeficient patients. Our objective is to provide a general overview of the parvovirus B19 infection and its characteristics in immunocompromised patients and to summarize updated information regarding the clinicopathologic features, pathobiology, and laboratory diagnosis of this subject. The pathologist should be aware of the wide spectrum of manifestations of parvovirus B19 infection depending on the patient's hematologic and immunologic status.

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40

Sattler, F. R. "Effects of Pharmacological Doses of Nandrolone Decanoate and Progressive Resistance Training in Immunodeficient Patients Infected with Human Immunodeficiency Virus." Journal of Clinical Endocrinology & Metabolism 84, no. 4 (April 1, 1999): 1268–76. http://dx.doi.org/10.1210/jc.84.4.1268.

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List, A. F., F. A. Greco, and L. B. Vogler. "Lymphoproliferative diseases in immunocompromised hosts: the role of Epstein-Barr virus." Journal of Clinical Oncology 5, no. 10 (October 1987): 1673–89. http://dx.doi.org/10.1200/jco.1987.5.10.1673.

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Epstein-Barr virus (EBV) is a ubiquitous transforming virus of the herpes group showing tropism for B lymphocytes. Primary infection in normal hosts results in a transient lymphoproliferative disorder, acute infectious mononucleosis (IM), that is restricted by cytotoxic and suppressive lymphocytes. However, in the immunodeficient host, EBV-induced lymphoproliferation may behave in a biologically malignant fashion. Patients with primary immunodeficiencies and those with immune incompetence resulting from suppressive therapy in allograft transplantation or infection with human immunodeficiency virus (HIV) have EBV-related illness ranging from fulminant mononucleosis and invasive polyclonal B cell hyperplasia to monoclonal B cell malignancies. While the direct link between EBV and malignant B cell proliferation in these patients has not been elucidated, the association has been increasingly recognized with improved techniques of viral detection. Clinical management can be guided by the location and extent of tumor, histologic features, and clonality. Regional and node-based polyclonal proliferations may respond to prompt reduction of immunosuppressive therapy and efforts to interrupt the replicative cycle with antiviral agents. Systemic cytotoxic therapy often leads to further immunosuppression and should be reserved for patients with progressive disease, advanced visceral involvement, and monoclonal lymphoid malignancies.

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Andreo, Ursula, Ype P. de Jong, Margaret A. Scull, Jing W. Xiao, Koen Vercauteren, Corrine Quirk, Michiel C. Mommersteeg, et al. "Analysis of Hepatitis C Virus Particle Heterogeneity in Immunodeficient Human Liver Chimeric fah-/- Mice." Cellular and Molecular Gastroenterology and Hepatology 4, no. 3 (November 2017): 405–17. http://dx.doi.org/10.1016/j.jcmgh.2017.07.002.

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43

Baroncini, Luca, Simon Bredl, Kadzioch P. Nicole, and Roberto F. Speck. "The Humanized Mouse Model: What Added Value Does It Offer for HIV Research?" Pathogens 12, no. 4 (April 17, 2023): 608. http://dx.doi.org/10.3390/pathogens12040608.

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In the early 2000s, novel humanized mouse models based on the transplantation of human hematopoietic stem and progenitor cells (HSPCs) into immunocompromised mice were introduced (hu mice). The human HSPCs gave rise to a lymphoid system of human origin. The HIV research community has greatly benefitted from these hu mice. Since human immunodeficiency virus (HIV) type 1 infection results in a high-titer disseminated HIV infection, hu mice have been of great value for all types of HIV research from pathogenesis to novel therapies. Since the first description of this new generation of hu mice, great efforts have been expended to improve humanization by creating other immunodeficient mouse models or supplementing mice with human transgenes to improve human engraftment. Many labs have their own customized hu mouse models, making comparisons quite difficult. Here, we discuss the different hu mouse models in the context of specific research questions in order to define which characteristics should be considered when determining which hu mouse model is appropriate for the question posed. We strongly believe that researchers must first define their research question and then determine whether a hu mouse model exists, allowing the research question to be studied.

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Chao, Hengjun, and Christopher E. Walsh. "Induction of tolerance to human factor VIII in mice." Blood 97, no. 10 (May 15, 2001): 3311–12. http://dx.doi.org/10.1182/blood.v97.10.3311.

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Abstract This paper reports loss of human factor VIII (hFVIII) inhibitory antibody in immunocompetent C57BL/6 mice. High-titer anti-hFVIII antibody developed in the mice within 7 to 14 days of intraportal administration of adeno-associated virus (AAV) carrying FVIII that coincided with a reduction in plasma hFVIII antigen. Bethesda titers (> 100 units) persisted relatively unchanged for 9 to 10 months. Unexpectedly, at 10 months after injection of the virus, hFVIII protein (up to 59 ng/mL) was detected in 3 mice at the same time as disappearance of hFVIII inhibitor. The level of hFVIII was similar to that found in immunodeficient mice receiving the same dose of recombinant AAV carrying hFVIII without hFVIII inhibitor. These results suggest that tolerance to hFVIII can be induced by sustained expression of hFVIII in a mouse model. Further elucidation of this observation may affect use of FVIII gene transfer in the treatment of inhibitor-positive patients with hemophilia A.

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Koyanagi, Y., Y. Tanaka, J. Kira, M. Ito, K. Hioki, N. Misawa, Y. Kawano, et al. "Primary human immunodeficiency virus type 1 viremia and central nervous system invasion in a novel hu-PBL-immunodeficient mouse strain." Journal of virology 71, no. 3 (1997): 2417–24. http://dx.doi.org/10.1128/jvi.71.3.2417-2424.1997.

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Delbue, Serena, Mariano Ferraresso, Luciana Ghio, Camilla Carloni, Silvia Carluccio, Mirco Belingheri, Alberto Edefonti, and Pasquale Ferrante. "A Review on JC Virus Infection in Kidney Transplant Recipients." Clinical and Developmental Immunology 2013 (2013): 1–7. http://dx.doi.org/10.1155/2013/926391.

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The polyomavirus (PyV), JC virus (JCV), is a small nonenveloped DNA virus that asymptomatically infects about 80% of healthy adults and establishes latency in the kidney tissue. In case of immunodeficient hosts, JCV can lytically infect the oligodendrocytes, causing a fatal demyelinating disease, known as progressive multifocal leukoencephalopathy (PML). Although the reactivation of another human PyV, BK virus (BKV), is relatively common and its association with the polyomavirus associated nephropathy (PyVAN) following renal transplantation is proven, JCV replication and its impact on graft function and survival are less well studied. Here we describe the biology of JCV and its pathological features and we review the literature regarding the JCV infection analyzed in the setting of transplantations.

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Kwant-Mitchell, Amanda, Ali A. Ashkar, and Kenneth L. Rosenthal. "Mucosal Innate and Adaptive Immune Responses against Herpes Simplex Virus Type 2 in a Humanized Mouse Model." Journal of Virology 83, no. 20 (August 5, 2009): 10664–76. http://dx.doi.org/10.1128/jvi.02584-08.

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ABSTRACT Genital herpes, caused by herpes simplex virus type 2 (HSV-2), is one of the most prevalent sexually transmitted diseases worldwide and a risk factor for acquiring human immunodeficiency virus. Although many vaccine candidates have shown promising results in animal models, they have failed to be effective in human trials. In this study, a humanized mouse strain was evaluated as a potential preclinical model for studying human immune responses to HSV-2 infection and vaccination. Immunodeficient mouse strains were examined for their abilities to develop human innate and adaptive immune cells after transplantation of human umbilical cord stem cells. A RAG2−/− γc−/− mouse strain with a BALB/c background was chosen as the most appropriate model and was then examined for its ability to mount innate and adaptive immune responses to intravaginal HSV-2 infection and immunization. After primary infection, human cells in the lymph nodes were able to generate a protective innate immune response and produce gamma interferon (IFN-γ). After intravaginal immunization and infection, human T cells and NK cells were found in the genital tract and iliac lymph nodes. In addition, human T cells in the spleen, lymph nodes, and vaginal tract were able to respond to stimulation with HSV-2 antigens by replicating and producing IFN-γ. Human B cells were also able to produce HSV-2-specific immunoglobulin G. These adaptive responses were also shown to be protective and reduce local viral replication in the genital tract. This approach provides a means for studying human immune responses in vivo using a small-animal model and may become an important preclinical tool.

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Park, Frank, Kazuo Ohashi, and Mark A. Kay. "Therapeutic levels of human factor VIII and IX using HIV-1–based lentiviral vectors in mouse liver." Blood 96, no. 3 (August 1, 2000): 1173–76. http://dx.doi.org/10.1182/blood.v96.3.1173.

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Abstract Lentiviral vectors have the potential to play an important role in hemophilia gene therapy. The present study used human immunodeficiency virus (HIV)-based lentiviral vectors containing an EF1 enhancer/promoter driving human factors VIII (hFVIII) or IX (hFIX) complementary DNA expression for portal vein injection into C57Bl/6 mice. Increasing doses of hFIX-expressing lentivirus resulted in a dose-dependent, sustained increase in serum hFIX levels up to approximately 50-60 ng/mL. Partial hepatectomy resulted in a 4- to 6-fold increase (P < 0.005) in serum hFIX of up to 350 ng/mL compared with the nonhepatectomized counterparts. The expression of plasma hFVIII reached 30 ng/mL (15% of normal) but was transient as the plasma levels fell concomitant with the formation of anti-hFVIII antibodies. However, hFVIII levels were persistent in immunodeficient C57Bl/6 scid mice, suggesting humoral immunity-limited gene expression in immunocompetent mice. This study demonstrates that lentiviral vectors can produce therapeutic levels of coagulation factors in vivo, which can be enhanced with hepatocellular proliferation.

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Park, Frank, Kazuo Ohashi, and Mark A. Kay. "Therapeutic levels of human factor VIII and IX using HIV-1–based lentiviral vectors in mouse liver." Blood 96, no. 3 (August 1, 2000): 1173–76. http://dx.doi.org/10.1182/blood.v96.3.1173.015k34_1173_1176.

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Lentiviral vectors have the potential to play an important role in hemophilia gene therapy. The present study used human immunodeficiency virus (HIV)-based lentiviral vectors containing an EF1 enhancer/promoter driving human factors VIII (hFVIII) or IX (hFIX) complementary DNA expression for portal vein injection into C57Bl/6 mice. Increasing doses of hFIX-expressing lentivirus resulted in a dose-dependent, sustained increase in serum hFIX levels up to approximately 50-60 ng/mL. Partial hepatectomy resulted in a 4- to 6-fold increase (P < 0.005) in serum hFIX of up to 350 ng/mL compared with the nonhepatectomized counterparts. The expression of plasma hFVIII reached 30 ng/mL (15% of normal) but was transient as the plasma levels fell concomitant with the formation of anti-hFVIII antibodies. However, hFVIII levels were persistent in immunodeficient C57Bl/6 scid mice, suggesting humoral immunity-limited gene expression in immunocompetent mice. This study demonstrates that lentiviral vectors can produce therapeutic levels of coagulation factors in vivo, which can be enhanced with hepatocellular proliferation.

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Krishnakumar, Vinodhini, Siva Durairajan, Kalichamy Alagarasu, Min Li, and Aditya Dash. "Recent Updates on Mouse Models for Human Immunodeficiency, Influenza, and Dengue Viral Infections." Viruses 11, no. 3 (March 13, 2019): 252. http://dx.doi.org/10.3390/v11030252.

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Abstract:

Well-developed mouse models are important for understanding the pathogenesis and progression of immunological response to viral infections in humans. Moreover, to test vaccines, anti-viral drugs and therapeutic agents, mouse models are fundamental for preclinical investigations. Human viruses, however, seldom infect mice due to differences in the cellular receptors used by the viruses for entry, as well as in the innate immune responses in mice and humans. In other words, a species barrier exists when using mouse models for investigating human viral infections. Developing transgenic (Tg) mice models expressing the human genes coding for viral entry receptors and knock-out (KO) mice models devoid of components involved in the innate immune response have, to some extent, overcome this barrier. Humanized mouse models are a third approach, developed by engrafting functional human cells and tissues into immunodeficient mice. They are becoming indispensable for analyzing human viral diseases since they nearly recapitulate the human disease. These mouse models also serve to test the efficacy of vaccines and antiviral agents. This review provides an update on the Tg, KO, and humanized mouse models that are used in studies investigating the pathogenesis of three important human-specific viruses, namely human immunodeficiency (HIV) virus 1, influenza, and dengue.

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Journal articles on the topic 'Human Immunodeficient Virus'

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