Journal articles: 'HIV pathogenicity'

1

Kurimura, K. "Pathogenicity of human immunodeficiency virus(HIV)." Uirusu 41, no. 2 (1991): 77–84. http://dx.doi.org/10.2222/jsv.41.77.

Full text

APA, Harvard, Vancouver, ISO, and other styles

2

Borek, F. "HIV molecular organization, pathogenicity and treatment." Journal of Immunological Methods 172, no. 1 (June 1994): 136–37. http://dx.doi.org/10.1016/0022-1759(94)90389-1.

Full text

APA, Harvard, Vancouver, ISO, and other styles

3

Sweet, SP. "Selection and pathogenicity ofCandida albicansin HIV infection." Oral Diseases 3, S1 (May 1997): S88—S95. http://dx.doi.org/10.1111/j.1601-0825.1997.tb00383.x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

4

Khan, Nabab, Xuesong Chen, and Jonathan D. Geiger. "Role of Divalent Cations in HIV-1 Replication and Pathogenicity." Viruses 12, no. 4 (April 21, 2020): 471. http://dx.doi.org/10.3390/v12040471.

Full text

Abstract:

Divalent cations are essential for life and are fundamentally important coordinators of cellular metabolism, cell growth, host-pathogen interactions, and cell death. Specifically, for human immunodeficiency virus type-1 (HIV-1), divalent cations are required for interactions between viral and host factors that govern HIV-1 replication and pathogenicity. Homeostatic regulation of divalent cations’ levels and actions appear to change as HIV-1 infection progresses and as changes occur between HIV-1 and the host. In people living with HIV-1, dietary supplementation with divalent cations may increase HIV-1 replication, whereas cation chelation may suppress HIV-1 replication and decrease disease progression. Here, we review literature on the roles of zinc (Zn2+), iron (Fe2+), manganese (Mn2+), magnesium (Mg2+), selenium (Se2+), and copper (Cu2+) in HIV-1 replication and pathogenicity, as well as evidence that divalent cation levels and actions may be targeted therapeutically in people living with HIV-1.

APA, Harvard, Vancouver, ISO, and other styles

5

Battaglia, Piero A., Santina Zito, Antonella Macchini, and Franca Gigliani. "A Drosophila model of HIV-Tat-related pathogenicity." Journal of Cell Science 114, no. 15 (August 1, 2001): 2787–94. http://dx.doi.org/10.1242/jcs.114.15.2787.

Full text

Abstract:

To analyze the mechanism of Tat-mediated HIV pathogenicity, we produced a Drosophila melanogaster strain transgenic for HIV-tat gene and induced the expression of the protein during Drosophila development. By in vitro and in vivo experiments, we demonstrated that Tat specifically binds to tubulin via the MAP-binding domain of tubulin, and that this interaction delays the polymerization of tubulin and induces a premature stop to microtubule-dependent cytoplasmic streaming. The delay in the polymerization of microtubules, the tracks for the transport of the axes determinants, alters the positioning of the dorso-ventral axis as shown by the mislocalization of Gurken and Kinesin in oocyte of Drosophila after Tat induction. These results validate the use of Drosophila as a tool to study the molecular mechanism of viral gene products and suggest that Tat-tubulin interaction is responsible for neurodegenerative diseases associated with AIDS.

APA, Harvard, Vancouver, ISO, and other styles

6

Duus, Karen M., Eric D. Miller, Jonathan A. Smith, Grigoriy I. Kovalev, and Lishan Su. "Separation of Human Immunodeficiency Virus Type 1 Replication from nef-Mediated Pathogenesis in the Human Thymus." Journal of Virology 75, no. 8 (April 15, 2001): 3916–24. http://dx.doi.org/10.1128/jvi.75.8.3916-3924.2001.

Full text

Abstract:

ABSTRACT Human immunodeficiency virus type 1 (HIV-1) is frequently attenuated after long-term culture in vitro. The attenuation process probably involves mutations of functions required for replication and pathogenicity in vivo. Analysis of attenuated HIV-1 for replication and pathogenicity in vivo will help to define these functions. In this study, we examined the pathogenicity of an attenuated HIV-1 isolate in a laboratory worker accidentally exposed to a laboratory-adapted HIV-1 isolate. Using heterochimeric SCID-hu Thy/Liv mice as an in vivo model, we previously defined HIV-1 env determinants (HXB/LW) that reverted to replicate in vivo (L. Su, H. Kaneshima, M. L. Bonyhadi, R. Lee, J. Auten, A. Wolf, B. Du, L. Rabin, B. H. Hahn, E. Terwilliger, and J. M. McCune, Virology 227:46–52, 1997). Here we further demonstrate that HIV-1 replication in vivo can be separated from its pathogenic activity, in that the HXB/LW virus replicated to high levels in SCID-hu Thy/Liv mice, with no significant thymocyte depletion. Restoration of the nef gene in the recombinant HXB/LW genome restored its pathogenic activity, with no significant effect on HIV-1 replication in the thymus. Our results suggest that in vitro-attenuated HIV-1 lacks determinants for pathogenicity as well as for replication in vivo. Our data indicate that (i) the replication defect can be recovered in vivo by mutations in the envgene, without an associated pathogenic phenotype, and (ii)nef can function in the HXB/LW clone as a pathogenic factor that does not enhance HIV-1 replication in the thymus. Furthermore, the HXB/LW virus may be used to study mechanisms of HIV-1nef-mediated pathogenesis in vivo.

APA, Harvard, Vancouver, ISO, and other styles

7

Dwek, Nicole Zitzmann, Joanne M. O'Leary and Raymond A. "Glycobiology against viruses: Antiviral drug discovery." Biochemist 28, no. 3 (June 1, 2006): 23–26. http://dx.doi.org/10.1042/bio02803023.

Full text

Abstract:

Most aspects of glycobiology play important roles in the ‘life’ of viruses, for example in the correct folding of their envelope glycoproteins as well as in immune representation and escape. The pathogenicity of three major human pathogens, HCV (hepatitis C virus), HBV (hepatitis B virus) and HIV, which collectively infect more than 560 million people worldwide, is dependent on their glycoproteins. As the sugars (or glycans) that the viruses rely on are supplied by the host cell, we can exploit our knowledge of glycobiology to target this apparent Achilles' heel of these viruses.

APA, Harvard, Vancouver, ISO, and other styles

8

Romani, Bizhan, and Susan Engelbrecht. "Human immunodeficiency virus type 1 Vpr: functions and molecular interactions." Journal of General Virology 90, no. 8 (August 1, 2009): 1795–805. http://dx.doi.org/10.1099/vir.0.011726-0.

Full text

Abstract:

Human immunodeficiency virus type 1 (HIV-1) viral protein R (Vpr) is an accessory protein that interacts with a number of cellular and viral proteins. The functions of many of these interactions in the pathogenesis of HIV-1 have been identified. Deletion of the vpr gene reduces the virulence of HIV-1 dramatically, indicating the importance of this protein for the virus. This review describes the current findings on several established functions of HIV-1 Vpr and some possible roles proposed for this protein. Because Vpr exploits cellular proteins and pathways to influence the biology of HIV-1, understanding the functions of Vpr usually involves the study of cellular pathways. Several functions of Vpr are attributed to the virion-incorporated protein, but some of them are attributed to the expression of Vpr in HIV-1-infected cells. The structure of Vpr may be key to understanding the variety of its interactions. Due to the critical role of Vpr in HIV-1 pathogenicity, study of the interactions between Vpr and cellular proteins may help us to understand the mechanism(s) of HIV-1 pathogenicity.

APA, Harvard, Vancouver, ISO, and other styles

9

Griffiths, PD. "Improved understanding of human genetic control of HIV pathogenicity." Reviews in Medical Virology 15, no. 1 (2004): 1–2. http://dx.doi.org/10.1002/rmv.459.

Full text

APA, Harvard, Vancouver, ISO, and other styles

10

Jupsa-Mbiandou, Stéphanie, Samuel Fosso, Edimo Billé, Tito T. Mélachio-Tanekou, Gideon Ajeagah-Aghaindum, Hugues C. Nana-Djeunga, Albert Samé-Ekobo, and Flobert Njiokou. "Pathogenicity and non-opportunistic character of Blastocystis spp.: a hospital-based survey in Central Cameroon." Journal of Infection in Developing Countries 12, no. 05 (May 31, 2018): 373–79. http://dx.doi.org/10.3855/jidc.10122.

Full text

Abstract:

Introduction: Blastocystis spp. is a protist found in humans. Although usually the most frequent protozoa found in stool samples of both symptomatic and healthy subjects, its pathogenic or rather opportunistic role is yet to be clearly elucidated. To attempt to fill this gap, a cross-sectional study was conducted to compare the frequency of Blastocystis spp. in HIV positive (HIV+) versus HIV negative (HIV-) individuals in four health facilities of the Center Region of Cameroon. Methodology: Stool samples were collected from 283 HIV positive and 245 HIV negative subjects and analyzed using direct diagnostic tests. Results: A total of 46 (8.7%) individuals were found infected with Blastocystis spp., including 6.7% HIV positive and 11.0% HIV negative. This species was more frequent in urban and semi-urban areas than in rural areas, but evenly distributed among genders and age groups as well as among all sectors of activity. The prevalence of Blastocystis spp. (11.3%) was higher in HIV+ patients with a CD4 count ≥ 500 cells / mm3, but no significant difference was found among HIV clinical stages. Likewise prevalence, the mean number of cysts per gram of stool was similar between HIV positive and HIV negative individuals. People infected with Blastocystis spp. showed diverse clinical signs, but only flatulence was significantly more prevalent. The frequencies of these clinical signs were not related to HIV status. Conclusion: No clear relationship links the infection with Blastocystis spp. to HIV, although its presence was associated with digestive disorder, suggesting that this parasite might not be opportunist.

APA, Harvard, Vancouver, ISO, and other styles

11

Davenport, Yunji W., Anthony P. West, and Pamela J. Bjorkman. "Structure of an HIV-2 gp120 in Complex with CD4." Journal of Virology 90, no. 4 (November 25, 2015): 2112–18. http://dx.doi.org/10.1128/jvi.02678-15.

Full text

Abstract:

HIV-2 is a nonpandemic form of the virus causing AIDS, and the majority of HIV-2-infected patients exhibit long-term nonprogression. The HIV-1 and HIV-2 envelope glycoproteins, the sole targets of neutralizing antibodies, share 30 to 40% identity. As a first step in understanding the reduced pathogenicity of HIV-2, we solved a 3.0-Å structure of an HIV-2 gp120 bound to the host receptor CD4, which reveals structural similarity to HIV-1 gp120 despite divergence in amino acid sequence.

APA, Harvard, Vancouver, ISO, and other styles

12

Jakobsen, Martin R., Anne Ellett, Melissa J. Churchill, and Paul R. Gorry. "Viral tropism, fitness and pathogenicity of HIV-1 subtype C." Future Virology 5, no. 2 (March 2010): 219–31. http://dx.doi.org/10.2217/fvl.09.77.

Full text

APA, Harvard, Vancouver, ISO, and other styles

13

Pekovic, Drasko D., Mervyn Gornitsky, Djordje Ajdukovic, Jean-Marie Dupuy, Jean-Paul Chausseau, Jean Michaud, Normand Lapointe, et al. "Pathogenicity of HIV in lymphatic organs of patients with AIDS." Journal of Pathology 152, no. 1 (May 1987): 31–35. http://dx.doi.org/10.1002/path.1711520105.

Full text

APA, Harvard, Vancouver, ISO, and other styles

14

Keppler, Oliver T., Ina Allespach, Lismarie Schüller, David Fenard, Warner C. Greene, and Oliver T. Fackler. "Rodent Cells Support Key Functions of the Human Immunodeficiency Virus Type 1 Pathogenicity Factor Nef." Journal of Virology 79, no. 3 (February 1, 2005): 1655–65. http://dx.doi.org/10.1128/jvi.79.3.1655-1665.2005.

Full text

Abstract:

ABSTRACT After infection with human immunodeficiency virus (HIV), progression toward immunodeficiency is governed by a complex interplay of viral and host determinants. The viral accessory protein Nef is a key factor for the development of AIDS. Strains of HIV and simian immunodeficiency virus that lack functional nef genes either do not induce AIDS or do so only after a significant delay. The validity of a transgenic-small-animal model for de novo infection by HIV will depend on its ability to recapitulate the actions of critical factors of viral pathogenicity, such as Nef. We assessed the ability of rat, mouse, and hamster cells to support key effector functions of Nef. In cell lines from rodents, the subcellular distribution of wild-type HIV type 1 strain SF2 Nef and mutants was comparable to that in human cells. Nef downregulated human CD4 from the cell surface, was associated with p21-activated kinase activity, and enhanced the infectivity of HIV-1 virions. Importantly, these Nef-induced effects, as well as the downregulation of rat CD4 and major histocompatibility complex class I molecules, could also be demonstrated in primary T lymphocytes and macrophages from human CD4-transgenic rats. Thus, HIV-1 Nef exerts key functions in rodent cells. In line with our ongoing efforts to establish a transgenic-rat model of HIV disease, these results indicate that important aspects of viral pathogenesis could be addressed in a transgenic-rodent model permissive for de novo infection and that such a model would be valuable for evaluating the function of Nef in vivo.

APA, Harvard, Vancouver, ISO, and other styles

15

Wacleche, V. S., P. Ancuta, J. P. Goulet, A. Gosselin, M. C. Gaudreau, and J. P. Routy. "Pathogenicity of CD16 + monocyte-derived dendritic cells during HIV-1 infection." Journal of Virus Eradication 1 (December 2015): 36. http://dx.doi.org/10.1016/s2055-6640(20)31399-6.

Full text

APA, Harvard, Vancouver, ISO, and other styles

16

Gorry, Paul R., Melissa Churchill, Jennifer Learmont, Catherine Cherry, Wayne B. Dyer, Steven L. Wesselingh, and John S. Sullivan. "Replication-Dependent Pathogenicity of Attenuated nef-Deleted HIV-1 In Vivo." JAIDS Journal of Acquired Immune Deficiency Syndromes 46, no. 4 (December 2007): 390–94. http://dx.doi.org/10.1097/qai.0b013e31815aba08.

Full text

APA, Harvard, Vancouver, ISO, and other styles

17

Churchill, Melissa J., David I. Rhodes, Jennifer C. Learmont, John S. Sullivan, Steven L. Wesselingh, Ian R. C. Cooke, Nicholas J. Deacon, and Paul R. Gorry. "Longitudinal Analysis of Human Immunodeficiency Virus Type 1 nef/Long Terminal Repeat Sequences in a Cohort of Long-Term Survivors Infected from a Single Source." Journal of Virology 80, no. 2 (January 15, 2006): 1047–52. http://dx.doi.org/10.1128/jvi.80.2.1047-1052.2006.

Full text

Abstract:

ABSTRACT We studied the evolution of human immunodeficiency virus type 1 (HIV-1) in a cohort of long-term survivors infected with an attenuated strain of HIV-1 acquired from a single source. Although the cohort members experienced differing clinical courses, we demonstrate similar evolution of HIV-1 nef/long-terminal repeat (LTR) sequences, characterized by progressive sequence deletions tending toward a minimal nef/LTR structure that retains only sequence elements required for viral replication. The in vivo pathogenicity of attenuated HIV-1 is therefore dictated by viral and/or host factors other than those that impose a unidirectional selection pressure on the nef/LTR region of the HIV-1 genome.

APA, Harvard, Vancouver, ISO, and other styles

18

Abrantes, Pedro M. D. S., Randall Fisher, Patrick J. D. Bouic, Carole P. McArthur, Burtram C. Fielding, and Charlene W. J. Africa. "HPLC-MS identification and expression of Candida drug-resistance proteins from African HIV-infected patients." AIMS Microbiology 7, no. 3 (2021): 320–35. http://dx.doi.org/10.3934/microbiol.2021020.

Full text

Abstract:

<abstract> <p>The objective of this study was to elucidate the proteomic mechanisms of drug resistance in HIV-infected African patients. Cell membrane fractions from forty oral <italic>Candida</italic> isolates isolated from African HIV-positive patients were analysed using HPLC-MS with the aim of identifying proteins associated with their pathogenicity and drug resistance. Heat shock proteins that mediate the fungicidal activity of salivary peptides were found in all tested <italic>Candida</italic> fractions, with pH-responsive proteins associated with increased pathogenicity only being present in the three most commonly isolated species. ABC multidrug transporter efflux pumps and estrogen binding proteins were only found in <italic>C. albicans</italic> fractions, while ergosterol biosynthesis proteins were identified in four species. The combination of various adherence, invasion, upregulation and efflux pump mechanisms appear to be instrumental for the <italic>Candida</italic> host colonization and drug resistance emergence in HIV-infected individuals.</p> </abstract>

APA, Harvard, Vancouver, ISO, and other styles

19

Parra, Micaela, Natalia Laufer, Julieta M. Manrique, Leandro R. Jones, and Jorge Quarleri. "Phylogenetic Diversity in Core Region of Hepatitis C Virus Genotype 1a as a Factor Associated with Fibrosis Severity in HIV-1-Coinfected Patients." BioMed Research International 2017 (2017): 1–12. http://dx.doi.org/10.1155/2017/1728456.

Full text

Abstract:

High hepatitis C virus (HCV) genetic diversity impacts infectivity/pathogenicity, influencing chronic liver disease progression associated with fibrosis degrees and hepatocellular carcinoma. HCV core protein is crucial in cell-growth regulation and host-gene expression. Liver fibrosis is accelerated by unknown mechanisms in human immunodeficiency virus-1- (HIV-1-) coinfected individuals. We aimed to study whether well-defined HCV-1a core polymorphisms and genetic heterogeneity are related to fibrosis in a highly homogeneous group of interferon-treated HIV-HCV-coinfected patients. Genetic heterogeneity was weighed by Faith’s phylogenetic diversity (PD), which has been little studied in HCV. Eighteen HCV/HIV-coinfected patients presenting different liver fibrosis stages before anti-HCV treatment-initiation were recruited. Sampling at baseline and during and after treatment was performed up to 72 weeks. At inter/intrahost level, HCV-1a populations were studied using molecular cloning and Sanger sequencing. Over 400 complete HCV-1a core sequences encompassing 573 positions of C were obtained. Amino acid substitutions found previously at positions 70 and 91 of HCV-1b core region were not observed. However, HCV genetic heterogeneity was higher in mild than in severe fibrosis cases. These results suggest a potential utility of PD as a virus-related factor associated with chronic hepatitis C progression. These observations should be reassessed in larger cohorts to corroborate our findings and assess other potential covariates.

APA, Harvard, Vancouver, ISO, and other styles

20

Prost, Stéphane, Mikael le Dantec, Sylvie Augé, Roger Le GRAND, Sonia Derdouch, Gwenaelle Auregan, Nicole Déglon, et al. "Human and Simian Immunodeficiency Viruses De-Regulate Early Hematopoiesis through a Novel Nef/PPAR-γ/STAT5 Signaling Pathway." Blood 112, no. 11 (November 16, 2008): 5389. http://dx.doi.org/10.1182/blood.v112.11.5389.5389.

Full text

Abstract:

Abstract Infection of primates by HIV-1 and SIV induces multiple hematological abnormalities of central hematopoietic origin. Although these defects greatly contribute to the pathophysiology of HIV-1 infection, the molecular basis for altered BM function remains unknown. Here we show that when cynomolgus macaques were infected with SIV, the multipotent potential of their hematopoietic progenitor cells was lost, and this correlated with down regulation of STAT5A and STAT5B expression. However, forced expression of STAT5B entirely rescued the multipotent potential of the hematopoietic progenitor cells. In addition, an accessory viral protein required for efficient SIV and HIV replication and pathogenicity, “Negative factor” (Nef), was essential for <SIV-mediated impairment of the multipotent potential of hematopoietic progenitors ex vivo and in vivo. This newly uncovered property of Nef was both conserved between HIV-1 and SIV strains and entirely dependent upon the presence of PPARγ in targeted cells. Further, PPARγ agonists mimicked Nef activity by inhibiting STAT5A and STAT5B expression and hampering the functionality of hematopoietic progenitors both ex vivo and in vivo. These findings have extended the role of Nef in the pathogenicity of HIV-1 and SIV and reveal a pivotal role for the PPARγ/STAT5 pathway in the regulation of early hematopoiesis. This study may provide a basis for investigating the potential therapeutic benefits of PPARγ antagonists in both patients with AIDS and individuals with hematopoietic disorders.

APA, Harvard, Vancouver, ISO, and other styles

21

Popper, Stephen J., Abdoulaye Dieng Sarr, Karin U. Travers, Aissatou Guèye‐Ndiaye, Souleymane Mboup, Myron E. Essex, and Phyllis J. Kanki. "Lower Human Immunodeficiency Virus (HIV) Type 2 Viral Load Reflects the Difference in Pathogenicity of HIV‐1 and HIV‐2." Journal of Infectious Diseases 180, no. 4 (October 1999): 1116–21. http://dx.doi.org/10.1086/315010.

Full text

APA, Harvard, Vancouver, ISO, and other styles

22

Aldrovandi, Grace M., Lianying Gao, Gregory Bristol, and Jerome A. Zack. "Regions of Human Immunodeficiency Virus Type 1nef Required for Function In Vivo." Journal of Virology 72, no. 9 (September 1, 1998): 7032–39. http://dx.doi.org/10.1128/jvi.72.9.7032-7039.1998.

Full text

Abstract:

ABSTRACT In vivo studies in monkeys and humans have indicated that immunodeficiency viruses with Nef deleted are nonpathogenic in immunocompetent hosts, and this has motivated a search for live attenuated vaccine candidates. However, the mechanisms of action of Nef remain elusive. To define the regions of human immunodeficiency virus type 1 (HIV-1) Nef which mediate in vivo pathogenicity, a series of mutated isogenic viruses were inoculated into human thymic implants in SCID-hu mice. Mutation of several regions, including the myristoylation site at the second glycine and a region encompassing amino acids 41 through 49 of Nef, profoundly affected pathogenicity. Surprisingly, mutations of prolines in either of the two distant PXXP SH3 binding domains did not affect pathogenicity, indicating that these regions are not required for Nef activity in developing T-lineage cells. These data suggest that some functions of Nef described in vitro may not be relevant for in vivo pathogenicity.

APA, Harvard, Vancouver, ISO, and other styles

23

Brandt, Ludivine, Sara Cristinelli, and Angela Ciuffi. "Single-Cell Analysis Reveals Heterogeneity of Virus Infection, Pathogenicity, and Host Responses: HIV as a Pioneering Example." Annual Review of Virology 7, no. 1 (September 29, 2020): 333–50. http://dx.doi.org/10.1146/annurev-virology-021820-102458.

Full text

Abstract:

While analyses of cell populations provide averaged information about viral infections, single-cell analyses offer individual consideration, thereby revealing a broad spectrum of diversity as well as identifying extreme phenotypes that can be exploited to further understand the complex virus-host interplay. Single-cell technologies applied in the context of human immunodeficiency virus (HIV) infection proved to be valuable tools to help uncover specific biomarkers as well as novel candidate players in virus-host interactions. This review aims at providing an updated overview of single-cell analyses in the field of HIV and acquired knowledge on HIV infection, latency, and host response. Although HIV is a pioneering example, similar single-cell approaches have proven to be valuable for elucidating the behavior and virus-host interplay in a range of other viruses.

APA, Harvard, Vancouver, ISO, and other styles

24

Cavaleiro, Rita, Ana E. Sousa, Ana Loureiro, and Rui M. M. Victorino. "Marked immunosuppressive effects of the HIV-2 envelope protein in spite of the lower HIV-2 pathogenicity." AIDS 14, no. 17 (December 2000): 2679–86. http://dx.doi.org/10.1097/00002030-200012010-00007.

Full text

APA, Harvard, Vancouver, ISO, and other styles

25

&NA;. "Herpesviruses: to blame or not to blame in the pathogenicity of HIV?" Inpharma Weekly &NA;, no. 997 (July 1995): 4. http://dx.doi.org/10.2165/00128413-199509970-00003.

Full text

APA, Harvard, Vancouver, ISO, and other styles

26

Gürtler, Lutz G. "Effect of Antiretroviral HIV Therapy on Hepatitis B Virus Replication and Pathogenicity." Intervirology 57, no. 3-4 (2014): 212–17. http://dx.doi.org/10.1159/000360942.

Full text

APA, Harvard, Vancouver, ISO, and other styles

27

Gorry, Paul R., Dale A. McPhee, Erin Verity, Wayne B. Dyer, Steven L. Wesselingh, Jennifer Learmont, John S. Sullivan, et al. "Pathogenicity and immunogenicity of attenuated, nef-deleted HIV-1 strains in vivo." Retrovirology 4, no. 1 (2007): 66. http://dx.doi.org/10.1186/1742-4690-4-66.

Full text

APA, Harvard, Vancouver, ISO, and other styles

28

Levin, Aviad, Zvi Hayouka, Ruth Brack-Werner, David J. Volsky, Assaf Friedler, and Abraham Loyter. "Novel regulation of HIV-1 replication and pathogenicity: Rev inhibition of integration." Protein Engineering, Design and Selection 22, no. 12 (October 29, 2009): 753–63. http://dx.doi.org/10.1093/protein/gzp060.

Full text

APA, Harvard, Vancouver, ISO, and other styles

29

Popper, Stephen J., Abdoulaye Dieng Sarr, Aïssatou Guèye-Ndiaye, Souleymane Mboup, Myron E. Essex, and Phyllis J. Kanki. "Low Plasma Human Immunodeficiency Virus Type 2 Viral Load Is Independent of Proviral Load: Low Virus Production In Vivo." Journal of Virology 74, no. 3 (February 1, 2000): 1554–57. http://dx.doi.org/10.1128/jvi.74.3.1554-1557.2000.

Full text

Abstract:

ABSTRACT Levels of virus in the plasma are closely related to the pathogenicity of human immunodeficiency virus type 1 (HIV-1). HIV-2 is much less pathogenic than HIV-1, and infection with HIV-2 leads to significantly lower plasma viral load. To identify the source of this difference, we measured both viral RNA and proviral DNA in matched samples from 34 HIV-2-infected individuals. Nearly half had undetectable viral RNA loads (<100 copies/ml), but levels of proviral DNA were relatively high and confirmed that quantities of provirus in HIV-1 and HIV-2 infection were similar. Overall, HIV-2 proviral DNA load did not correlate with viral RNA load, and higher viral RNA load was associated with increased production of plasma virus from the proviral template. These results suggest that low viral load in HIV-2 infection is due to decreased rates of viral production, rather than differences in target cell infectivity.

APA, Harvard, Vancouver, ISO, and other styles

30

Kunzi, MS, and JE Groopman. "Identification of a novel human immunodeficiency virus strain cytopathic to megakaryocytic cells." Blood 81, no. 12 (June 15, 1993): 3336–42. http://dx.doi.org/10.1182/blood.v81.12.3336.3336.

Full text

Abstract:

Abstract Impaired megakaryocytopoiesis may be a contributing factor to thrombocytopenia associated with human immunodeficiency virus (HIV) infection. Because HIV isolates differ in their host range and pathogenicity, we investigated whether HIV strains with demonstrable cell tropism and increased cytopathicity for megakaryocytes could be derived from the blood of thrombocytopenic HIV-infected individuals. We derived a strain, HIV-WW, from the peripheral blood of an individual with severe thrombocytopenia and found the virus to be highly and specifically cytotoxic to CMK and DAMI megakaryocytic cells. CMK and DAMI cells were not permissive for the virus and HIV-WW induced cytopathicity for these megakaryocytic cells did not depend on viral replication. The CD4 N-terminus-binding domain of the HIV gp120 envelope protein did not appear to be involved in determining the cytopathic phenomenon. HIV may impair megakaryocytopoiesis through interactions at the cell surface in some cases rather than through viral entry and intracellular replication.

APA, Harvard, Vancouver, ISO, and other styles

31

Kunzi, MS, and JE Groopman. "Identification of a novel human immunodeficiency virus strain cytopathic to megakaryocytic cells." Blood 81, no. 12 (June 15, 1993): 3336–42. http://dx.doi.org/10.1182/blood.v81.12.3336.bloodjournal81123336.

Full text

Abstract:

Impaired megakaryocytopoiesis may be a contributing factor to thrombocytopenia associated with human immunodeficiency virus (HIV) infection. Because HIV isolates differ in their host range and pathogenicity, we investigated whether HIV strains with demonstrable cell tropism and increased cytopathicity for megakaryocytes could be derived from the blood of thrombocytopenic HIV-infected individuals. We derived a strain, HIV-WW, from the peripheral blood of an individual with severe thrombocytopenia and found the virus to be highly and specifically cytotoxic to CMK and DAMI megakaryocytic cells. CMK and DAMI cells were not permissive for the virus and HIV-WW induced cytopathicity for these megakaryocytic cells did not depend on viral replication. The CD4 N-terminus-binding domain of the HIV gp120 envelope protein did not appear to be involved in determining the cytopathic phenomenon. HIV may impair megakaryocytopoiesis through interactions at the cell surface in some cases rather than through viral entry and intracellular replication.

APA, Harvard, Vancouver, ISO, and other styles

32

Jekle, Andreas, Oliver T. Keppler, Erik De Clercq, Dominique Schols, Mark Weinstein, and Mark A. Goldsmith. "In Vivo Evolution of Human Immunodeficiency Virus Type 1 toward Increased Pathogenicity through CXCR4-Mediated Killing of Uninfected CD4 T Cells." Journal of Virology 77, no. 10 (May 15, 2003): 5846–54. http://dx.doi.org/10.1128/jvi.77.10.5846-5854.2003.

Full text

Abstract:

ABSTRACT The destruction of the immune system by progressive loss of CD4 T cells is the hallmark of AIDS. CCR5-dependent (R5) human immunodeficiency virus type 1 (HIV-1) isolates predominate in the early, asymptomatic stages of HIV-1 infection, while CXCR4-dependent (X4) isolates typically emerge at later stages, frequently coinciding with a rapid decline in CD4 T cells. Lymphocyte killing in vivo primarily occurs through apoptosis, but the importance of apoptosis of HIV-1-infected cells relative to apoptosis of uninfected bystander cells is controversial. Here we show that in human lymphoid tissues ex vivo, apoptosis of uninfected bystander CD4 T cells is a major mechanism of lymphocyte depletion caused by X4 HIV-1 strains but is only a minor mechanism of depletion by R5 strains. Further, X4 HIV-1-induced bystander apoptosis requires the interaction of the viral envelope glycoprotein gp120 with the CXCR4 coreceptor on CD4 T cells. These results emphasize the contribution of bystander apoptosis to HIV-1 cytotoxicity and suggest that in association with a coreceptor switch in HIV disease, T-cell killing evolves from an infection-restricted stage to generalized toxicity that involves a high degree of bystander apoptosis.

APA, Harvard, Vancouver, ISO, and other styles

33

McGettigan, James P., Roger J. Pomerantz, Catherine A. Siler, Philip M. McKenna, Heather D. Foley, B. Dietzschold, and Matthias J. Schnell. "Second-Generation Rabies Virus-Based Vaccine Vectors Expressing Human Immunodeficiency Virus Type 1 Gag Have Greatly Reduced Pathogenicity but Are Highly Immunogenic." Journal of Virology 77, no. 1 (January 1, 2003): 237–44. http://dx.doi.org/10.1128/jvi.77.1.237-244.2003.

Full text

Abstract:

ABSTRACT Rabies virus (RV) vaccine strain-based vectors show great promise as vaccines against other viral diseases such as human immunodeficiency virus type 1 (HIV-1) infection and hepatitis C, but a low residual pathogenicity remains a concern for their use. Here we describe several highly attenuated second-generation RV-based vaccine vehicles expressing HIV-1 Gag. For this approach, we modified the previously described RV vaccine vector SPBN by replacing the arginine at position 333 (R333) within the RV glycoprotein (G) with glutamic acid (E333), deleting 43 amino acids of the RV G cytoplasmic domain (CD), or combining the R333 exchange and the CD deletion. In addition, we constructed a new RV vector that expresses HIV-1 Gag from an RV transcription unit upstream of the RV phosphoprotein gene (BNSP-Gag) instead of upstream of the G gene. As expected and as demonstrated for SPBN-Gag, all vaccine vehicles were apathogenic after peripheral administration. However, the new, second-generation vaccine vectors containing modifications in the RV G were also apathogenic after intracranial infection with 105 infectious particles, and BNSP-Gag produced a 50%-reduced mortality in mice. Of note, the observed attenuation of pathogenicity did not result in either the attenuation of the humoral response against the RV G or the previously observed robust cellular response against HIV-1 Gag. These findings demonstrate that very safe and highly effective RV-based vaccines can be constructed and further emphasize their potential utility as efficacious antiviral vaccines.

APA, Harvard, Vancouver, ISO, and other styles

34

Dai, Lue, and Mario Stevenson. "A Novel Motif in HIV-1 Nef That Regulates MIP-1β Chemokine Release in Macrophages." Journal of Virology 84, no. 16 (May 26, 2010): 8327–31. http://dx.doi.org/10.1128/jvi.00741-10.

Full text

Abstract:

ABSTRACT All primate lentiviruses encode Nef, an accessory protein that is important for viral pathogenicity in vivo. Lentiviral Nef proteins regulate the release of chemokines (MIP-1 α/β) from infected macrophages, thereby enhancing virus dissemination (S. Swingler, A. Mann, J. Jacque, B. Brichacek, V. G. Sasseville, K. Williams, A. A. Lackner, E. N. Janoff, R. Wang, D. Fisher, and M. Stevenson, Nat. Med. 5:997-1003, 1999). In the current study, we have identified a novel domain within Nef (K92EK) that is required for Nef-dependent MIP-1β production by infected macrophages. Mutations in this domain abrogated MIP-1β induction but did not affect other Nef-ascribed activities, such as CD4 or major histocompatibility complex (MHC) class Ι downregulation. This further underscores Nef as a modular protein with genetically separable activities that may contribute to its role in viral replication and pathogenicity.

APA, Harvard, Vancouver, ISO, and other styles

35

Sivaraman, Vijay, Liguo Zhang, Eric G. Meissner, Jerry L. Jeffrey, and Lishan Su. "The Heptad Repeat 2 Domain Is a Major Determinant for Enhanced Human Immunodeficiency Virus Type 1 (HIV-1) Fusion and Pathogenicity of a Highly Pathogenic HIV-1 Env." Journal of Virology 83, no. 22 (September 2, 2009): 11715–25. http://dx.doi.org/10.1128/jvi.00649-09.

Full text

Abstract:

ABSTRACT Human immunodeficiency virus type 1 (HIV-1)-mediated depletion of CD4+ lymphocytes in an infected individual is the hallmark of progression to AIDS. However, the mechanism for this depletion remains unclear. To identify mechanisms of HIV-1-mediated CD4 T-cell death, two similar viral isolates obtained from a rapid progressor patient with significantly different pathogenic phenotypes were studied. One isolate (R3A) demonstrates enhanced pathogenesis in both in vivo models and relevant ex vivo lymphoid organ model systems compared to another isolate, R3B. The pathogenic determinants were previously mapped to the V5-gp41 envelope region, correlating functionally with enhanced fusion activity and elevated CXCR4 binding affinity. To further elucidate specific differences between R3A and R3B within the V5-gp41 domains that enhance CD4 depletion, R3A-R3B chimeras to study the V5-gp41 region were developed. Our data demonstrate that six residues in the ectodomain of R3A provide the major determinant for both enhanced Env-cell fusion and pathogenicity. Furthermore, three amino acid differences in the heptad repeat 2 (HR-2) domain of R3A determined its fusion activity and significantly elevated its pathogenic activity. The chimeric viruses with enhanced fusion activity, but not elevated CXCR4 affinity, correlated with high pathogenicity in the thymus organ. We conclude that the functional domain of a highly pathogenic HIV-1 Env is determined by mutations in the HR-2 region that contribute to enhanced fusion and CD4 T-cell depletion.

APA, Harvard, Vancouver, ISO, and other styles

36

Alatortseva, G. I., M. N. Nosik, L. N. Nesterenko, I. I. Amiantova, V. V. Dotsenko, L. N. Luhverchik, M. V. Zhuckina, V. U. Kabargina, E. N. Kudryavtseva, and V. V. Zverev. "Study of Antigenic properties of Human immunodeficiency Virus NEF protein Recombinant Analog." Epidemiology and Vaccine Prevention 15, no. 3 (June 20, 2016): 83–93. http://dx.doi.org/10.31631/2073-3046-2016-15-3-83-93.

Full text

Abstract:

Protein p27/p25 is a product of HIV nef gene and is a multifunctional factor of HIV pathogenicity. Antigenic properties of recombinant NEF polypeptide which includes N-terminal fragment of HIV-1 p27 protein fused to E. coli ß-galactosidase were studied by serological and virological methods. The interaction was shown between recombinant NEF antigen and serums of HIV-positive individuals by ELISA, Western blot and line immunoassay. There was no interaction with sera of healthy individuals. The antigen specificity of recombinant antigen was shown in the reactions with commercial HIV-1 p27/p25 protein analog and with polyclonal antibodies to synthetic peptides corresponding to N-, C-terminal regions of HIV-1 p27/p25 protein. The interaction between IgG of rabbits immunized with recombinant NEF antigen and viral antigens was shown by indirect immunofluorescence and neutralizing assays. Thus it was proven the possibility of using recombinant NEF protein as an antigen for diagnostic and experimental purposes.

APA, Harvard, Vancouver, ISO, and other styles

37

Caobi, Allen, Madhavan Nair, and Andrea D. Raymond. "Extracellular Vesicles in the Pathogenesis of Viral Infections in Humans." Viruses 12, no. 10 (October 21, 2020): 1200. http://dx.doi.org/10.3390/v12101200.

Full text

Abstract:

Most cells can release extracellular vesicles (EVs), membrane vesicles containing various proteins, nucleic acids, enzymes, and signaling molecules. The exchange of EVs between cells facilitates intercellular communication, amplification of cellular responses, immune response modulation, and perhaps alterations in viral pathogenicity. EVs serve a dual role in inhibiting or enhancing viral infection and pathogenesis. This review examines the current literature on EVs to explore the complex role of EVs in the enhancement, inhibition, and potential use as a nanotherapeutic against clinically relevant viruses, focusing on neurotropic viruses: Zika virus (ZIKV) and human immunodeficiency virus (HIV). Overall, this review’s scope will elaborate on EV-based mechanisms, which impact viral pathogenicity, facilitate viral spread, and modulate antiviral immune responses.

APA, Harvard, Vancouver, ISO, and other styles

38

CALLAHAN, LARRY. "HIV-1 Virion-Cell Interactions: An Electrostatic Model of Pathogenicity and Syncytium Formation." AIDS Research and Human Retroviruses 10, no. 3 (March 1994): 231–33. http://dx.doi.org/10.1089/aid.1994.10.231.

Full text

APA, Harvard, Vancouver, ISO, and other styles

39

XIANG, ZHENG, KOYA ARIYOSHI, ANDREW WILKINS, F. DIAS, HILTON WHITTLE, and JUDITH BREUER. "HIV Type 2 Pathogenicity Is Not Related to Subtype in Rural Guinea Bissau." AIDS Research and Human Retroviruses 13, no. 6 (April 10, 1997): 501–5. http://dx.doi.org/10.1089/aid.1997.13.501.

Full text

APA, Harvard, Vancouver, ISO, and other styles

40

Ma, Yuanlin, Zuguo Yu, Runbin Tang, Xianhua Xie, Guosheng Han, and Vo V. Anh. "Phylogenetic Analysis of HIV-1 Genomes Based on the Position-Weighted K-mers Method." Entropy 22, no. 2 (February 23, 2020): 255. http://dx.doi.org/10.3390/e22020255.

Full text

Abstract:

HIV-1 viruses, which are predominant in the family of HIV viruses, have strong pathogenicity and infectivity. They can evolve into many different variants in a very short time. In this study, we propose a new and effective alignment-free method for the phylogenetic analysis of HIV-1 viruses using complete genome sequences. Our method combines the position distribution information and the counts of the k-mers together. We also propose a metric to determine the optimal k value. We name our method the Position-Weighted k-mers (PWkmer) method. Validation and comparison with the Robinson–Foulds distance method and the modified bootstrap method on a benchmark dataset show that our method is reliable for the phylogenetic analysis of HIV-1 viruses. PWkmer can resolve within-group variations for different known subtypes of Group M of HIV-1 viruses. This method is simple and computationally fast for whole genome phylogenetic analysis.

APA, Harvard, Vancouver, ISO, and other styles

41

Novembre, Francis J., Juliette de Rosayro, Soumya Nidtha, Shawn P. O'Neil, Terri R. Gibson, Tammy Evans-Strickfaden, Clyde E. Hart, and Harold M. McClure. "Rapid CD4+ T-Cell Loss Induced by Human Immunodeficiency Virus Type 1NC in Uninfected and Previously Infected Chimpanzees." Journal of Virology 75, no. 3 (February 1, 2001): 1533–39. http://dx.doi.org/10.1128/jvi.75.3.1533-1539.2001.

Full text

Abstract:

ABSTRACT To investigate the pathogenicity of a virus originating in a chimpanzee with AIDS (C499), two chimpanzees were inoculated with a plasma-derived isolate termed human immunodeficiency virus type 1NC (HIV-1NC). A previously uninfected chimpanzee, C534, experienced rapid peripheral CD4+ T-cell loss to fewer than 26 cells/μl by 14 weeks after infection. CD4+ T-cell depletion was associated with high plasma HIV-1 loads but a low virus burden in the peripheral lymph node. The second chimpanzee, C459, infected 13 years previously with HIV-1LAV, experienced a more protracted course of peripheral CD4+ T-cell loss after HIV-1NCinoculation, resulting in fewer than 200 cells/μl by 96 weeks postinoculation. The quantities of viral RNA in the plasma and peripheral lymph node from C459 were below the lower limits of detection prior to inoculation with HIV-1NC but were significantly and persistently increased after superinfection, with HIV-1NC representing the predominant viral genotype. These results show that viruses derived from C499 are more pathogenic for chimpanzees than any other HIV-1 isolates described to date.

APA, Harvard, Vancouver, ISO, and other styles

42

Gelderblom, Hans, Hilmar Reupke, Thorsten Winkel, Rudolf Kunze, and Georg Pauli. "MHC-Antigens: Constituents of the Envelopes of Human and Simian Immunodeficiency." Zeitschrift für Naturforschung C 42, no. 11-12 (December 1, 1987): 1328–34. http://dx.doi.org/10.1515/znc-1987-11-1230.

Full text

Abstract:

Immunoelectron microscopy was applied to study the antigenic make-up of human and simian immunodeficiency viruses (HIV, SIV) grown in cells expressing either MHC class I (Molt-3) or MHC class I and II (H9) antigens. A variety of antibodies directed against the surface glycopro tein gpl20 of HIV and against MHC class I and II antigens were employed. Consistent with earlier observations on the loss of HIV envelope components, gp120 was only weakly demonstra ble on the mature virion. MHC class I determinants were present regularly in small amounts on HIV and SIV. Class II antigens, e.g. HLA-DR were found in high density on HIV and SIV grown in H9 cells, but were absent, as expected, on virus grown in Molt-3 cells. These cellular surface antigens are con stituents of the virion. The presence of MHC class II antigens in virus preparations used for diagnostic purposes might explain some of the false positive results in HIV serology. Possible biological implications of these virus associated cellular antigens for the pathogenicity of HIV are discussed.

APA, Harvard, Vancouver, ISO, and other styles

43

Becker, Yechiel. "Retrovirus and filovirus “immunosuppressive motif” and the evolution of virus pathogenicity in HIV-1, HIV-2, and ebola viruses." Virus Genes 11, no. 2-3 (June 1995): 191–95. http://dx.doi.org/10.1007/bf01728658.

Full text

APA, Harvard, Vancouver, ISO, and other styles

44

LACAZ, Carlos da Silva, Elisabeth Maria HEINS-VACCARI, Giovanna L. HERNÁNDEZ-ARRIAGADA, Eduardo Lacaz MARTINS, Célia A. L. PREARO, Simone Miwa CORIM, and Marilena dos Anjos MARTINS. "Primary cutaneous cryptococcosis due to Cryptococcus neoformans var. gattii serotype B, in an immunocompetent patient." Revista do Instituto de Medicina Tropical de São Paulo 44, no. 4 (July 2002): 225–28. http://dx.doi.org/10.1590/s0036-46652002000400008.

Full text

Abstract:

The authors report a male patient, a seller with no detected immunosuppression, with an extensive ulcerated skin lesion localized on the left forearm, caused by Cryptococcus neoformans var. gattii serotype B. Oral treatment with fluconazole was successful. A review of the literature showed the rarity of this localization in HIV-negative patients. In contrast, skin lesions frequently occurs in HIV-positive patients, with Cryptococcus neoformans var. neoformans serotype A predominating as the etiological agent. In this paper, the pathogenicity of C. neoformans to skin lesions in patients immunocompromised or not, is discussed, showing the efficacy of fluconazole for the treatment of these processes.

APA, Harvard, Vancouver, ISO, and other styles

45

van der Ende, M. E., C. Guillon, P. H. M. Boers, R. A. Gruters, P. Racz, K. Tenner-Racz, A. D. M. E. Osterhaus, and M. Schutten. "Broadening of coreceptor usage by human immunodeficiency virus type 2 does not correlate with increased pathogenicity in an in vivo model." Microbiology 81, no. 2 (February 1, 2000): 507–13. http://dx.doi.org/10.1099/0022-1317-81-2-507.

Full text

Abstract:

The pathogenic properties of four primary human immunodeficiency virus type 2 (HIV-2) isolates and two primary HIV-2 biological clones were studied in an in vivo human-to-mouse chimeric model. The cell-associated viral load and the ability to reduce the severity of the induced graft-versus-host disease symptoms, the CD4/CD8 ratio and the level of repopulation of the mouse tissues by the graft, were determined. All HIV-2 strains, irrespective of their in vitro biological phenotype, replicated to high titres and significantly reduced graft-versus-host disease symptoms as well as the CD4/CD8 ratios. Reduction of graft repopulation caused by infection with the respective HIV-2 strains showed that the in vitro replication rate, syncytium-inducing capacity and ability to infect human macrophages did influence the in vivo pathogenic potential whereas broadening of coreceptor usage did not.

APA, Harvard, Vancouver, ISO, and other styles

46

Carl, Silke, Thomas C. Greenough, Mandy Krumbiegel, Michael Greenberg, Jacek Skowronski, John L. Sullivan, and Frank Kirchhoff. "Modulation of Different Human Immunodeficiency Virus Type 1 Nef Functions during Progression to AIDS." Journal of Virology 75, no. 8 (April 15, 2001): 3657–65. http://dx.doi.org/10.1128/jvi.75.8.3657-3665.2001.

Full text

Abstract:

ABSTRACT The human immunodeficiency virus type 1 (HIV-1) Nef protein has several independent functions that might contribute to efficient viral replication in vivo. Since HIV-1 adapts rapidly to its host environment, we investigated if different Nef properties are associated with disease progression. Functional analysis revealed thatnef alleles obtained during late stages of infection did not efficiently downmodulate class I major histocompatibility complex but were highly active in the stimulation of viral replication. In comparison, functional activity in downregulation of CD4 and enhancement of HIV-1 infectivity were maintained or enhanced after AIDS progression. Our results demonstrate that various Nef activities are modulated during the course of HIV-1 infection to maintain high viral loads at different stages of disease progression. These findings suggest that all in vitro Nef functions investigated contribute to AIDS pathogenesis and indicate that nef variants with increased pathogenicity emerge in a significant number of HIV-1-infected individuals.

APA, Harvard, Vancouver, ISO, and other styles

47

Guillon, Christophe, Marchina E. van der Ende, Patrick H. M. Boers, Rob A. Gruters, Martin Schutten, and Albert D. M. E. Osterhaus. "Coreceptor Usage of Human Immunodeficiency Virus Type 2 Primary Isolates and Biological Clones Is Broad and Does Not Correlate with Their Syncytium-Inducing Capacities." Journal of Virology 72, no. 7 (July 1, 1998): 6260–63. http://dx.doi.org/10.1128/jvi.72.7.6260-6263.1998.

Full text

Abstract:

ABSTRACT Entry of human immunodeficiency virus type 1 (HIV-1) into target cells is mediated by binding of the surface envelope glycoprotein to the CD4 molecule. Interaction of the resulting CD4-glycoprotein complex with α- or β-chemokine receptors, depending on the biological phenotype of the virus, then initiates the fusion process. Here, we show that primary HIV-2 isolates and biological clones, in contrast to those of HIV-1, may use a broad range of coreceptors, including CCR-1, CCR-3, CCR-5, and CXCR-4. The syncytium-inducing capacity of these viruses did not correlate with the ability to infect via CXCR-4 or any other coreceptor. One cell-free passage of the intermediate isolates in mitogen-stimulated, CD8+ cell-depleted peripheral blood mononuclear cells resulted in the outgrowth of variants with CCR-5 only, whereas the coreceptor usage of late and early isolates did not change. Since HIV-2 is less pathogenic in vivo than HIV-1, these data suggest that HIV pathogenicity in vivo is not directly related to the spectrum of coreceptors used in in vitro systems.

APA, Harvard, Vancouver, ISO, and other styles

48

Kessler, Harald H., Doris Deuretzbacher, Evelyn Stelzl, Elisabeth Daghofer, Brigitte I. Santner, and Egon Marth. "Determination of Human Immunodeficiency Virus Type 1 Subtypes by a Rapid Method Useful for the Routine Diagnostic Laboratory." Clinical Diagnostic Laboratory Immunology 8, no. 5 (September 1, 2001): 1018–20. http://dx.doi.org/10.1128/cdli.8.5.1018-1020.2001.

Full text

Abstract:

ABSTRACT The existence of human immunodeficiency virus type 1 (HIV-1) subtypes has many important implications for the global evolution of HIV and for the evaluation of pathogenicity, transmissibility, and candidate HIV vaccines. The aim of this study was to establish a rapid method for determination of HIV-1 subtypes useful for a routine diagnostic laboratory and to investigate the distribution of HIV-1 subtypes in Austrian patients. Samples were tested by a subtyping method based on a 1.3-kb sequence of the polymerase gene generated by a commercially available drug resistance assay. The generated sequence was subtyped by means of an HIV sequence database. Results of 74 routine samples revealed subtype B (71.6%) as the predominant subtype, followed by subtype A (13.5%) and subtype C (6.8%). Subtypes E, F, G, and AE (CM240) were also detected. This subtyping method was found to be very easy to handle, rapid, and inexpensive and has proved suitable for high-throughput routine diagnostic laboratories. The specific polymerase gene sequence, however, must be existent.

APA, Harvard, Vancouver, ISO, and other styles

49

Ivanov, Alexander V., Vladimir T. Valuev-Elliston, Olga N. Ivanova, Sergey N. Kochetkov, Elizaveta S. Starodubova, Birke Bartosch, and Maria G. Isaguliants. "Oxidative Stress during HIV Infection: Mechanisms and Consequences." Oxidative Medicine and Cellular Longevity 2016 (2016): 1–18. http://dx.doi.org/10.1155/2016/8910396.

Full text

Abstract:

It is generally acknowledged that reactive oxygen species (ROS) play crucial roles in a variety of natural processes in cells. If increased to levels which cannot be neutralized by the defense mechanisms, they damage biological molecules, alter their functions, and also act as signaling molecules thus generating a spectrum of pathologies. In this review, we summarize current data on oxidative stress markers associated with human immunodeficiency virus type-1 (HIV-1) infection, analyze mechanisms by which this virus triggers massive ROS production, and describe the status of various defense mechanisms of the infected host cell. In addition, we have scrutinized scarce data on the effect of ROS on HIV-1 replication. Finally, we present current state of knowledge on the redox alterations as crucial factors of HIV-1 pathogenicity, such as neurotoxicity and dementia, exhaustion of CD4+/CD8+T-cells, predisposition to lung infections, and certain side effects of the antiretroviral therapy, and compare them to the pathologies associated with the nitrosative stress.

APA, Harvard, Vancouver, ISO, and other styles

50

He, Sijia, and Yuntao Wu. "Relationships Between HIV-Mediated Chemokine Coreceptor Signaling, Cofilin Hyperactivation, Viral Tropism Switch and HIV-Mediated CD4 Depletion." Current HIV Research 17, no. 6 (January 3, 2020): 388–96. http://dx.doi.org/10.2174/1570162x17666191106112018.

Full text

Abstract:

: HIV infection causes CD4 depletion and immune deficiency. The virus infects CD4 T cells through binding to CD4 and one of the chemokine coreceptors, CXCR4 (X4) or CCR5 (R5). It has also been known that HIV tropism switch, from R5 to X4, is associated with rapid CD4 depletion, suggesting a key role of viral factors in driving CD4 depletion. However, the virological driver for HIV-mediated CD4 depletion has not been fully elucidated. We hypothesized that HIV-mediated chemokine coreceptor signaling, particularly chronic signaling through CXCR4, plays a major role in CD4 dysfunction and depletion; we also hypothesized that there is an R5X4 signaling (R5X4sig) viral subspecies, evolving from the natural replication course of R5-utilizing viruses, that is responsible for CD4 T cell depletion in R5 virus infection. To gain traction for our hypothesis, in this review, we discuss a recent finding from Cui and co-authors who described the rapid tropism switch and high pathogenicity of an HIV-1 R5 virus, CRF01_AE. We speculate that CRF01_AE may be the hypothetical R5X4sig viral species that is rapidly evolving towards the X4 phenotype. We also attempt to discuss the intricate relationships between HIV-mediated chemokine coreceptor signaling, viral tropism switch and HIV-mediated CD4 depletion, in hopes of providing a deeper understanding of HIV pathogenesis in blood CD4 T cells.

APA, Harvard, Vancouver, ISO, and other styles

Journal articles on the topic 'HIV pathogenicity'

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles