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Journal articles on the topic '(HIV-1)'

Author: Grafiati
Published: 4 June 2021
Last updated: 14 September 2024

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1

Tsukada, Kunihisa. "1. HIV-1 Infection." Nihon Naika Gakkai Zasshi 96, no. 11 (2007): 2442–49. http://dx.doi.org/10.2169/naika.96.2442.

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2

Asang, Corinna, Hans-J. Laws, Ortwin Adams, Jürgen Enczmann, Cornelia Feiterna-Sperling, Gundula Notheis, Bernd Buchholz, Arndt Borkhardt, and Jennifer Neubert. "HIV-1 seroreversion in HIV-1-infected children." AIDS 28, no. 4 (February 2014): 543–47. http://dx.doi.org/10.1097/qad.0000000000000065.

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3

Hansasuta, Pokrath, and Sarah L. Rowland-Jones. "HIV-1 transmission and acute HIV-1 infection." British Medical Bulletin 58, no. 1 (September 1, 2001): 109–27. http://dx.doi.org/10.1093/bmb/58.1.109.

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4

Curran, Kathryn, Jared M. Baeten, Thomas J. Coates, Ann Kurth, Nelly R. Mugo, and Connie Celum. "HIV-1 Prevention for HIV-1 Serodiscordant Couples." Current HIV/AIDS Reports 9, no. 2 (March 14, 2012): 160–70. http://dx.doi.org/10.1007/s11904-012-0114-z.

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5

Loussert-Ajaka, I., F. Brun-Vézinet, F. Simon, T. D. Ly, M. L. Chaix, S. Saragosti, A. M. Couroucé, and D. Ingrand. "HIV-1/HIV-2 seronegativity in HIV-1 subtype 0 infected patients." Lancet 343, no. 8910 (June 1994): 1393–94. http://dx.doi.org/10.1016/s0140-6736(94)92524-0.

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6

Fujiwara, Mamoru, and Masafumi Takiguchi. "HIV-1–specific CTLs effectively suppress replication of HIV-1 in HIV-1–infected macrophages." Blood 109, no. 11 (June 1, 2007): 4832–38. http://dx.doi.org/10.1182/blood-2006-07-037481.

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AbstractBoth CD4+ T cells and macrophages are major reservoirs of HIV-1. Previous study showed that HIV-1–specific cytolytic T lymphocytes (CTLs) hardly recognize HIV-1–infected CD4+ T cells because of Nef-mediated HLA class I down-regulation, suggesting that HIV-1 escapes from HIV-1–specific CTLs and continues to replicate in HIV-1–infected donors. On the other hand, the CTL recognition of HIV-1–infected macrophages and the effect of Nef-mediated HLA class I down-regulation on this recognition still remain unclear. We show a strong HIV-1 antigen presentation by HIV-1–infected macrophages. HIV-1–specific CTLs had strong abilities to suppress HIV-1R5 virus replication in HIV-1–infected macrophages and to kill HIV-1R5–infected macrophages. Nef-mediated HLA class I down-regulation minimally influenced the recognition of HIV-1–infected macrophages by HIV-1–specific CTLs. In addition, HIV-1–infected macrophages had a stronger ability to stimulate the proliferation of HIV-1–specific CTLs than HIV-1–infected CD4+ T cells. Thus, the effect of Nef-mediated HLA class I down-regulation was less critical with respect to the recognition by HIV-1–specific CTLs of HIV-infected macrophages than that of HIV-1–infected CD4+ T cells. These findings support the idea that the strong HIV-1 antigen presentation by HIV-1–infected macrophages is one of the mechanisms mediating effective induction of HIV-1–specific CTLs in the acute and early chronic phases of HIV-1 infection.
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7

Bradbury, Jane. "HIV-1-resistant individuals may lack HIV-1 coreceptor." Lancet 348, no. 9025 (August 1996): 463. http://dx.doi.org/10.1016/s0140-6736(05)64540-0.

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8

Shen, R., M. Raska, D. Bimczok, J. Novak, and P. D. Smith. "HIV-1 Envelope Glycan Moieties Modulate HIV-1 Transmission." Journal of Virology 88, no. 24 (October 1, 2014): 14258–67. http://dx.doi.org/10.1128/jvi.02164-14.

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9

Zeytinoğlu, Ayşın, Münevver Kayın, İmre Altuğlu, Deniz Gökengin, and Rüçhan Sertöz. "İki Anti-HIV Doğrulama Testinin Karşılaştırılması: Rekombinant HIV 1/2 “Line İmmunoassay” ve Geenius HIV 1/2 Doğrulama Testi." Mikrobiyoloji Bulteni 54, no. 4 (October 15, 2020): 613–18. http://dx.doi.org/10.5578/mb.69786.

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10

Joseph, J. Mehsen. "Testing (HIV-1)." Infection Control and Hospital Epidemiology 12, no. 8 (August 1991): 474–75. http://dx.doi.org/10.2307/30146877.

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11

Fultz, Patricia N. "HIV-1 superinfections." AIDS 18, no. 1 (January 2004): 115–19. http://dx.doi.org/10.1097/00002030-200401020-00014.

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12

Stevenson, Mario. "HIV-1 pathogenesis." Nature Medicine 9, no. 7 (July 2003): 853–60. http://dx.doi.org/10.1038/nm0703-853.

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13

Joseph, J. Mehsen. "Testing (HIV-1)." Infection Control and Hospital Epidemiology 12, no. 8 (August 1991): 474–75. http://dx.doi.org/10.1086/646385.

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14

Waters, Laura, and Erasmus Smit. "HIV-1 superinfection." Current Opinion in Infectious Diseases 25, no. 1 (February 2012): 42–50. http://dx.doi.org/10.1097/qco.0b013e32834ef5af.

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15

Harwig, Alex, Atze T. Das, and Ben Berkhout. "HIV-1 RNAs." Current Opinion in HIV and AIDS 10, no. 2 (March 2015): 103–9. http://dx.doi.org/10.1097/coh.0000000000000135.

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16

Pomerantz, Roger J. "HIV-1 reservoirs." Clinics in Laboratory Medicine 22, no. 3 (September 2002): 651–80. http://dx.doi.org/10.1016/s0272-2712(02)00005-7.

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17

Nakatani, Yoshihiro. "HIV-1 Transcription." Structure 10, no. 4 (April 2002): 443–44. http://dx.doi.org/10.1016/s0969-2126(02)00754-2.

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18

Strebel, Klaus. "HIV-1 Vpu." Molecular Cell 14, no. 2 (April 2004): 150–52. http://dx.doi.org/10.1016/s1097-2765(04)00205-9.

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19

Allen, Todd M., and Marcus Altfeld. "HIV-1 superinfection." Journal of Allergy and Clinical Immunology 112, no. 5 (November 2003): 829–35. http://dx.doi.org/10.1016/j.jaci.2003.08.037.

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20

Mok, Jacqueline. "HIV-1 INFECTION." Lancet 341, no. 8850 (April 1993): 930–31. http://dx.doi.org/10.1016/0140-6736(93)91217-a.

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21

Podzorski, Raymond P. "HIV-1 genotyping." Reviews in Medical Microbiology 14, no. 1 (January 2003): 25–34. http://dx.doi.org/10.1097/00013542-200301000-00003.

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22

Excler, Jean-Louis, Merlin L. Robb, and Jerome H. Kim. "HIV-1 vaccines." Human Vaccines & Immunotherapeutics 10, no. 6 (March 17, 2014): 1734–46. http://dx.doi.org/10.4161/hv.28462.

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23

Panos, George, and Mark Nelson. "HIV-1 tropism." Biomarkers in Medicine 1, no. 4 (December 2007): 473–81. http://dx.doi.org/10.2217/17520363.1.4.473.

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24

Visan, Ioana. "Restricting HIV-1." Nature Immunology 14, no. 11 (October 21, 2013): 1117. http://dx.doi.org/10.1038/ni.2753.

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25

Buckland, Jenny. "Silencing HIV-1." Nature Reviews Immunology 2, no. 7 (July 2002): 458. http://dx.doi.org/10.1038/nri849.

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26

NAVE, J. "HIV-1 inhibitor." Drug Discovery Today 1, no. 4 (April 1996): 170. http://dx.doi.org/10.1016/1359-6446(96)89068-4.

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27

Iwamoto, Aikichi, Noriaki Hosoya, and Ai Kawana-Tachikawa. "HIV-1 tropism." Protein & Cell 1, no. 6 (June 2010): 510–13. http://dx.doi.org/10.1007/s13238-010-0066-2.

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28

&NA;. "HIV-1 vaccine promising in children with HIV-1 infection." Inpharma Weekly &NA;, no. 1205 (September 1999): 10. http://dx.doi.org/10.2165/00128413-199912050-00016.

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29

Goto, Toshiyuki, Chizuko Morita, Taisuke Ashina, Kazuyoshi Ikuta, Shiro Kato, and Masuyo Nakal. "Localization of constituent proteins of HIV Type 1 (HIV-1)." Proceedings, annual meeting, Electron Microscopy Society of America 48, no. 3 (August 12, 1990): 340–41. http://dx.doi.org/10.1017/s0424820100159242.

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The localization of the constituent proteins of HIV-1 in the virions and HIV-1-infected cells was examined by indirect immuno-gold labeling with monoclonal antibodies (MoAb) to gag proteins (p18 and p24/p53), to elucidate viral formation of HIV.Persistently HIV-1 (HTLV—IIIB,LAV-1)-infected MT-4 and MOLT-4 cell lines and their cloned cell lines were used as infected cells. Mouse MoAb against HIV-1 gag p18 (V17) and p24/p53 (V107) were used. The cells were fixed with 0.5-1% glutar-aldehyde in phosphate-buffered saline (pH 7.2), dehydrated in ethanol and embedded in epoxy (at 45° Cor 60°C) or Lowicryl K4M resin (at −30°C). The sections were incubated in MoAb at room temperature for 1 h and then incubated in anti-mouse goat IgG conjugated with gold (IgG-gold, 5 or 15 nm; Janssen) for 40 min. After being washed, the sections were stained with uranyl acetate and lead citrate, and were observed in an electron microscope with a tilting apparatus.The spećific reactions with V17 and V107 were detected on HIV-1 particles and in the infected cells. No reactivity was noted between uninfected control cells and the MoAb, or between the infected cells and normal mouse serum. More than 97% of the HIV-1 particles embedded in epoxy resinat 60°C were labeled with gold after exclusion of the HIV particles that were attached to supporting film or completely embedded in the section (Fig. 1). Increased labeling was observed with Lowicryl (Fig. 2)and epoxy resin embedding at 45°C.
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30

Maeda, Yosuke, Keisuke Yusa, and Shinji Harada. "Enhanced infectivity of HIV-1 by X4 HIV-1 coinfection." Biochemical and Biophysical Research Communications 308, no. 4 (September 2003): 906–13. http://dx.doi.org/10.1016/s0006-291x(03)01498-0.

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31

Suzuki, Shintaro, Emiko Urano, Chie Hashimoto, Hiroshi Tsutsumi, Toru Nakahara, Tomohiro Tanaka, Yuta Nakanishi, et al. "Peptide HIV-1 Integrase Inhibitors from HIV-1 Gene Products." Journal of Medicinal Chemistry 53, no. 14 (July 22, 2010): 5356–60. http://dx.doi.org/10.1021/jm1003528.

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32

Reagan, KevinJ, CathyC Lile, Yair Devash, John Turner, Yu-Wen Hu, and C. Yong Kang. "Use of HIV-1 pol gene precursor to detect HIV-1 and HIV-2." Lancet 335, no. 8683 (January 1990): 236. http://dx.doi.org/10.1016/0140-6736(90)90338-6.

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33

Mourez, Thomas, Constance Delaugerre, Muriel Vray, Véronique Lemée, François Simon, and Jean-Christophe Plantier. "Comparison of the bioMérieux NucliSENS EasyQ HIV-1 v2.0–HIV-1 RNA quantification assay versus Abbott RealTime HIV-1 and Roche Cobas TaqMan HIV-1 v2.0 on current epidemic HIV-1 variants." Journal of Clinical Virology 71 (October 2015): 76–81. http://dx.doi.org/10.1016/j.jcv.2015.08.007.

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34

Araujo, Abelardo Q. C. "Neurological Aspects of HIV-1/HTLV-1 and HIV-1/HTLV-2 Coinfection." Pathogens 9, no. 4 (March 28, 2020): 250. http://dx.doi.org/10.3390/pathogens9040250.

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Simultaneous infection by human immunodeficiency viruses (HIV) and human T-lymphotropic viruses (HTLV) are not uncommon since they have similar means of transmission and are simultaneously endemic in many populations. Besides causing severe immune dysfunction, these viruses are neuropathogenic and can cause neurological diseases through direct and indirect mechanisms. Many pieces of evidence at present show that coinfection may alter the natural history of general and, more specifically, neurological disorders through different mechanisms. In this review, we summarize the current evidence on the influence of coinfection on the progression and outcome of neurological complications of HTLV-1/2 and HIV-1.
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35

&NA;. "HIV-1 expression inhibited by HIV-2." Inpharma Weekly &NA;, no. 1021 (January 1996): 10. http://dx.doi.org/10.2165/00128413-199610210-00015.

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36

Travis, J. "HIV-2 Offers Protection against HIV-1." Science News 147, no. 24 (June 17, 1995): 373. http://dx.doi.org/10.2307/3978894.

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37

Savall, R., X. Balanzo, J. L. Fernandez, F. Valls, and V. Soriano. "HIV-1 and HIV-2 in Spain." Sexually Transmitted Infections 68, no. 2 (April 1, 1992): 143. http://dx.doi.org/10.1136/sti.68.2.143.

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38

Hayes, R. J., P. G. Smith, François Denis, and Francis Barin. "SEROPOSITIVITY TO HIV-1 AND HIV-2." Lancet 329, no. 8543 (May 1987): 1199–200. http://dx.doi.org/10.1016/s0140-6736(87)92163-5.

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39

Sarr, Abdoulaye Dieng, Donald J. Hamel, Ibou Thior, Efi Kokkotou, Jean-Louis Sankalé, Richard G. Marlink, Eva-Marie Coll-Seck, et al. "HIV-1 and HIV-2 dual infection." AIDS 12, no. 2 (January 1998): 131–37. http://dx.doi.org/10.1097/00002030-199802000-00002.

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40

Weiss, Robin A., Paul R. Clapham, Jonathan N. Weber, Denise Whitby, Richard S. Tedder, Tim OʼConnor, Sophie Chamaret, and Luc Montagnier. "HIV-2 antisera cross-neutralize HIV-1." AIDS 2, no. 2 (April 1988): 95–100. http://dx.doi.org/10.1097/00002030-198804000-00004.

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41

Zanchetta, Marisa, Alessia Anselmi, Daniela Vendrame, Osvalda Rampon, Carlo Giaquinto, Antonio Mazza, Daniele Accapezzato, Vincenzo Barnaba, and Anita De Rossi. "Early Therapy in HIV-1-Infected Children: Effect on HIV-1 Dynamics and HIV-1-Specific Immune Response." Antiviral Therapy 13, no. 1 (January 2008): 47–56. http://dx.doi.org/10.1177/135965350801300105.

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Background Perinatal HIV-1 infection is acquired in the milieu of a developing immune system, leading to high levels of uncontrolled viral replication. Few data have been reported that address the viral dynamics and immunological response in infants who initiated aggressive antiretroviral therapy (ART) shortly after birth. Methods Six HIV-1-infected infants who started ART within 3 months of age were studied. The median follow-up was 61 months. Plasma HIV-1 RNA, cell-associated HIV-1 DNA, unspliced and multiply spliced HIV-1 mRNAs, HIV-1 antibodies, and CD4+ and CD8+ T-cell subsets were assessed in sequential peripheral blood samples. HIV-1 cellular immune response was measured by EliSpot assay. Results All children showed a decline in plasma viraemia to undetectable levels. HIV-1 DNA persisted in four children, but only two of these had detectable HIV-1 mRNA. All viral parameters remained persistently negative in two children. Only two children produced HIV-1 antibodies, while the others, after having lost maternal antibodies, remained seronegative. No HIV-1 cellular immune response was observed in any child. Therapy interruption was performed in two children: one HIV-1-seropositive and one HIV-1-seronegative with persistently undetectable levels of all viral parameters. Rebound of HIV-1 plasma viraemia in the seronegative child was more rapid and higher than that observed in the seropositive child. Conclusions Early ART treatment in infants modifies the natural course of infection by controlling HIV-1 replication and reducing viral load to below the threshold levels required for onset of HIV-1 immune response, but does not prevent the establishment of a reservoir of latently infected cells that precludes virus eradication.
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42

Mor, Orna, Yael Gozlan, Marina Wax, Fernando Mileguir, Avia Rakovsky, Bina Noy, Ella Mendelson, and Itzchak Levy. "Evaluation of the RealTime HIV-1, Xpert HIV-1, and Aptima HIV-1 Quant Dx Assays in Comparison to the NucliSens EasyQ HIV-1 v2.0 Assay for Quantification of HIV-1 Viral Load." Journal of Clinical Microbiology 53, no. 11 (August 19, 2015): 3458–65. http://dx.doi.org/10.1128/jcm.01806-15.

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HIV-1 RNA monitoring, both before and during antiretroviral therapy, is an integral part of HIV management worldwide. Measurements of HIV-1 viral loads are expected to assess the copy numbers of all common HIV-1 subtypes accurately and to be equally sensitive at different viral loads. In this study, we compared for the first time the performance of the NucliSens v2.0, RealTime HIV-1, Aptima HIV-1 Quant Dx, and Xpert HIV-1 viral load assays. Plasma samples (n= 404) were selected on the basis of their NucliSens v2.0 viral load results and HIV-1 subtypes. Concordance, linear regression, and Bland-Altman plots were assessed, and mixed-model analysis was utilized to compare the analytical performance of the assays for different HIV-1 subtypes and for low and high HIV-1 copy numbers. Overall, high concordance (>83.89%), high correlation values (Pearsonrvalues of >0.89), and good agreement were observed among all assays, although the Xpert and Aptima assays, which provided the most similar outputs (estimated mean viral loads of 2.67 log copies/ml [95% confidence interval [CI], 2.50 to 2.84 log copies/ml] and 2.68 log copies/ml [95% CI, 2.49 to 2.86 log copies/ml], respectively), correlated best with the RealTime assay (89.8% concordance, with Pearsonrvalues of 0.97 to 0.98). These three assays exhibited greater precision than the NucliSens v2.0 assay. All assays were equally sensitive for subtype B and AG/G samples and for samples with viral loads of 1.60 to 3.00 log copies/ml. The NucliSens v2.0 assay underestimated A1 samples and those with viral loads of >3.00 log copies/ml. The RealTime assay tended to underquantify subtype C (compared to the Xpert and Aptima assays) and subtype A1 samples. The Xpert and Aptima assays were equally efficient for detection of all subtypes and viral loads, which renders these new assays most suitable for clinical HIV laboratories.
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43

Ortiz de Lejarazu, R., V. Soriano, J. M. Eiros, M. Arias, and C. Toro. "HIV-1 Infection in Persistently HIV-1-Seronegative Individuals: More Reasons for HIV RNA Screening." Clinical Infectious Diseases 46, no. 5 (March 1, 2008): 785. http://dx.doi.org/10.1086/527569.

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44

Hønge, BL, S. Jespersen, C. Medina, DS Té, ZJ da Silva, M. Christiansen, B. Kjerulff, et al. "The challenge of discriminating between HIV-1, HIV-2 and HIV-1/2 dual infections." HIV Medicine 19, no. 6 (March 24, 2018): 403–10. http://dx.doi.org/10.1111/hiv.12606.

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45

Torresilla, Cynthia, Jean-Michel Mesnard, and Benoit Barbeau. "Reviving an Old HIV-1 Gene: The HIV-1 Antisense Protein." Current HIV Research 13, no. 2 (April 15, 2015): 117–24. http://dx.doi.org/10.2174/1570162x12666141202125943.

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46

Li, Hailong, Kristen A. McLaurin, Jessica M. Illenberger, Charles F. Mactutus, and Rosemarie M. Booze. "Microglial HIV-1 Expression: Role in HIV-1 Associated Neurocognitive Disorders." Viruses 13, no. 5 (May 17, 2021): 924. http://dx.doi.org/10.3390/v13050924.

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The persistence of HIV-1 viral reservoirs in the brain, despite treatment with combination antiretroviral therapy (cART), remains a critical roadblock for the development of a novel cure strategy for HIV-1. To enhance our understanding of viral reservoirs, two complementary studies were conducted to (1) evaluate the HIV-1 mRNA distribution pattern and major cell type expressing HIV-1 mRNA in the HIV-1 transgenic (Tg) rat, and (2) validate our findings by developing and critically testing a novel biological system to model active HIV-1 infection in the rat. First, a restricted, region-specific HIV-1 mRNA distribution pattern was observed in the HIV-1 Tg rat. Microglia were the predominant cell type expressing HIV-1 mRNA in the HIV-1 Tg rat. Second, we developed and critically tested a novel biological system to model key aspects of HIV-1 by infusing F344/N control rats with chimeric HIV (EcoHIV). In vitro, primary cultured microglia were treated with EcoHIV revealing prominent expression within 24 h of infection. In vivo, EcoHIV expression was observed seven days after stereotaxic injections. Following EcoHIV infection, microglia were the major cell type expressing HIV-1 mRNA, results that are consistent with observations in the HIV-1 Tg rat. Within eight weeks of infection, EcoHIV rats exhibited neurocognitive impairments and synaptic dysfunction, which may result from activation of the NogoA-NgR3/PirB-RhoA signaling pathway and/or neuroinflammation. Collectively, these studies enhance our understanding of HIV-1 viral reservoirs in the brain and offer a novel biological system to model HIV-associated neurocognitive disorders and associated comorbidities (i.e., drug abuse) in rats.
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47

Dimitrakopoulos, Antonios N. "Mixed Cryoglobulinemia in HIV-1 Infection: The Role of HIV-1." Annals of Internal Medicine 130, no. 3 (February 2, 1999): 226. http://dx.doi.org/10.7326/0003-4819-130-3-199902020-00027.

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48

Levin, Judith G., Mithun Mitra, Anjali Mascarenhas, and Karin Musier-Forsyth. "Role of HIV-1 nucleocapsid protein in HIV-1 reverse transcription." RNA Biology 7, no. 6 (November 2010): 754–74. http://dx.doi.org/10.4161/rna.7.6.14115.

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49

Campbell, Edward M., and Thomas J. Hope. "HIV-1 capsid: the multifaceted key player in HIV-1 infection." Nature Reviews Microbiology 13, no. 8 (July 16, 2015): 471–83. http://dx.doi.org/10.1038/nrmicro3503.

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50

Diedrich, Collin R., and JoAnne L. Flynn. "HIV-1/Mycobacterium tuberculosisCoinfection Immunology: How Does HIV-1 Exacerbate Tuberculosis?" Infection and Immunity 79, no. 4 (January 18, 2011): 1407–17. http://dx.doi.org/10.1128/iai.01126-10.

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ABSTRACTHuman immunodeficiency virus type 1 (HIV) andMycobacterium tuberculosishave become intertwined over the past few decades in a “syndemic” that exacerbates the morbidity and mortality associated with each pathogen alone. The severity of the coinfection has been extensively examined in clinical studies. The extrapolation of peripheral evidence from clinical studies has increased our basic understanding of how HIV increases susceptibility to TB. These studies have resulted in multiple hypotheses of how HIV exacerbates TB pathology through the manipulation of granulomas. Granulomas can be located in many tissues, most prominently the lungs and associated lymph nodes, and are made up of multiple immune cells that can actively containM. tuberculosis. Granuloma-based research involving both animal models and clinical studies is needed to confirm these hypotheses, which will further our understanding of this coinfection and may lead to better treatment options. This review examines the data that support each hypothesis of how HIV manipulates TB pathology while emphasizing a need for more tissue-based experiments.
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