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Journal articles on the topic 'Latent HIV'

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Author: Grafiati

Published: 10 December 2022

Last updated: 20 February 2023

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1

Stout, Jason E., Yanjue Wu, Christine S. Ho, April C. Pettit, Pei-Jean Feng, Dolly J. Katz, Smita Ghosh, Thara Venkatappa, and Ruiyan Luo. "Evaluating latent tuberculosis infection diagnostics using latent class analysis." Thorax 73, no. 11 (July 7, 2018): 1062–70. http://dx.doi.org/10.1136/thoraxjnl-2018-211715.

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BackgroundLack of a gold standard for latent TB infection has precluded direct measurement of test characteristics of the tuberculin skin test and interferon-γ release assays (QuantiFERON Gold In-Tube and T-SPOT.TB).ObjectiveWe estimated test sensitivity/specificity and latent TB infection prevalence in a prospective, US-based cohort of 10 740 participants at high risk for latent infection.MethodsBayesian latent class analysis was used to estimate test sensitivity/specificity and latent TB infection prevalence among subgroups based on age, foreign birth outside the USA and HIV infection.ResultsLatent TB infection prevalence varied from 4.0% among foreign-born, HIV-seronegative persons aged <5 years to 34.0% among foreign-born, HIV-seronegative persons aged ≥5 years. Test sensitivity ranged from 45.8% for the T-SPOT.TB among foreign-born, HIV-seropositive persons aged ≥5 years to 80.7% for the tuberculin skin test among foreign-born, HIV-seronegative persons aged ≥5 years. The skin test was less specific than either interferon-γ release assay, particularly among foreign-born populations (eg, the skin test had 70.0% specificity among foreign-born, HIV-seronegative persons aged ≥5 years vs 98.5% and 99.3% specificity for the QuantiFERON and T-SPOT.TB, respectively). The tuberculin skin test’s positive predictive value ranged from 10.0% among foreign-born children aged <5 years to 69.2% among foreign-born, HIV-seropositive persons aged ≥5 years; the positive predictive values of the QuantiFERON (41.4%) and T-SPOT.TB (77.5%) were also low among US-born, HIV-seropositive persons aged ≥5 years.ConclusionsThese data reinforce guidelines preferring interferon-γ release assays for foreign-born populations and recommending against screening populations at low risk for latent TB infection.Trial registration numberNCT01622140.

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2

Harrison, Charlotte. "Waking up latent HIV." Nature Reviews Drug Discovery 11, no. 9 (August 31, 2012): 674. http://dx.doi.org/10.1038/nrd3833.

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3

Cruz-Lorenzo, Emily, Nora-Guadalupe P. Ramirez, Jeon Lee, Sonali Pandhe, Lei Wang, Juan Hernandez-Doria, Adam M. Spivak, et al. "Host Cell Redox Alterations Promote Latent HIV-1 Reactivation through Atypical Transcription Factor Cooperativity." Viruses 14, no. 10 (October 18, 2022): 2288. http://dx.doi.org/10.3390/v14102288.

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Immune cell state alterations rewire HIV-1 gene expression, thereby influencing viral latency and reactivation, but the mechanisms are still unfolding. Here, using a screen approach on CD4+ T cell models of HIV-1 latency, we revealed Small Molecule Reactivators (SMOREs) with unique chemistries altering the CD4+ T cell state and consequently promoting latent HIV-1 transcription and reactivation through an unprecedented mechanism of action. SMOREs triggered rapid oxidative stress and activated a redox-responsive program composed of cell-signaling kinases (MEK-ERK axis) and atypical transcription factor (AP-1 and HIF-1α) cooperativity. SMOREs induced an unusual AP-1 phosphorylation signature to promote AP-1/HIF-1α binding to the latent HIV-1 proviral genome for its activation. Consistently, latent HIV-1 reactivation was compromised with pharmacologic inhibition of oxidative stress sensing or of cell-signaling kinases, and transcription factor’s loss of expression, thus functionally linking the host redox-responsive program to viral transcriptional rewiring. Notably, SMOREs induced the redox program in primary CD4+ T cells and reactivated latent HIV-1 in aviremic patient samples alone and in combination with known latency-reversing agents, thus providing physiological relevance. Our findings suggest that manipulation of redox-sensitive pathways could be exploited to alter the course of HIV-1 latency, thus rendering host cells responsive to help achieve a sterilizing cure.

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4

Cary, Daniele C., and B. Matija Peterlin. "Targeting the latent reservoir to achieve functional HIV cure." F1000Research 5 (May 26, 2016): 1009. http://dx.doi.org/10.12688/f1000research.8109.1.

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While highly active anti-retroviral therapy has greatly improved the lives of HIV-infected individuals, current treatments are unable to completely eradicate the virus. This is due to the presence of HIV latently infected cells which harbor transcriptionally silent HIV. Latent HIV does not replicate or produce viral proteins, thereby preventing efficient targeting by anti-retroviral drugs. Strategies to target the HIV latent reservoir include viral reactivation, enhancing host defense mechanisms, keeping latent HIV silent, and using gene therapy techniques to knock out or reactivate latent HIV. While research into each of these areas has yielded promising results, currently no one mechanism eradicates latent HIV. Instead, combinations of these approaches should be considered for a potential HIV functional cure.

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5

Mayanja, Edison, Livingstone S. Luboobi, Juma Kasozi, and Rebecca N. Nsubuga. "Mathematical Modelling of HIV-HCV Coinfection Dynamics in Absence of Therapy." Computational and Mathematical Methods in Medicine 2020 (October 6, 2020): 1–27. http://dx.doi.org/10.1155/2020/2106570.

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Globally, it is estimated that of the 36.7 million people infected with human immunodeficiency virus (HIV), 6.3% are coinfected with hepatitis C virus (HCV). Coinfection with HIV reduces the chance of HCV spontaneous clearance. In this work, we formulated and analysed a deterministic model to study the HIV and HCV coinfection dynamics in absence of therapy. Due to chronic stage of HCV infection being long, asymptomatic, and infectious, our model formulation was based on the splitting of the chronic stage into the following: before onset of cirrhosis and its complications and after onset of cirrhosis. We computed the basic reproduction numbers using the next generation matrix method. We performed numerical simulations to support the analytical results. We carried out sensitivity analysis to determine the relative importance of the different parameters influencing the HIV-HCV coinfection dynamics. The findings reveal that, in the long run, there is a substantial number of individuals coinfected with HIV and latent HCV. Therefore, HIV and latently HCV-infected individuals need to seek early treatment so as to slow down the progression of HIV to AIDS and latent HCV to advanced HCV.

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6

Jefferys, Stuart R., Samuel D. Burgos, Jackson J. Peterson, Sara R. Selitsky, Anne-Marie W. Turner, Lindsey I. James, Yi-Hsuan Tsai, et al. "Epigenomic characterization of latent HIV infection identifies latency regulating transcription factors." PLOS Pathogens 17, no. 2 (February 26, 2021): e1009346. http://dx.doi.org/10.1371/journal.ppat.1009346.

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Transcriptional silencing of HIV in CD4 T cells generates a reservoir of latently infected cells that can reseed infection after interruption of therapy. As such, these cells represent the principal barrier to curing HIV infection, but little is known about their characteristics. To further our understanding of the molecular mechanisms of latency, we characterized a primary cell model of HIV latency in which infected cells adopt heterogeneous transcriptional fates. In this model, we observed that latency is a stable, heritable state that is transmitted through cell division. Using Assay of Transposon-Accessible Chromatin sequencing (ATACseq) we found that latently infected cells exhibit greatly reduced proviral accessibility, indicating the presence of chromatin-based structural barriers to viral gene expression. By quantifying the activity of host cell transcription factors, we observe elevated activity of Forkhead and Kruppel-like factor transcription factors (TFs), and reduced activity of AP-1, RUNX and GATA TFs in latently infected cells. Interestingly, latency reversing agents with different mechanisms of action caused distinct patterns of chromatin reopening across the provirus. We observe that binding sites for the chromatin insulator CTCF are highly enriched in the differentially open chromatin of infected CD4 T cells. Furthermore, depletion of CTCF inhibited HIV latency, identifying this factor as playing a key role in the initiation or enforcement of latency. These data indicate that HIV latency develops preferentially in cells with a distinct pattern of TF activity that promotes a closed proviral structure and inhibits viral gene expression. Furthermore, these findings identify CTCF as a novel regulator of HIV latency.

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7

Destache, Christopher J. "HIV Latent Reservoir Cure Strategies." iScience Notes 1, no. 1 (October 15, 2016): 2. http://dx.doi.org/10.22580/2016/iscinote.2.

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8

Destache, Christopher J. "HIV Latent Reservoir Cure Strategies." iScience Notes 1, no. 1 (October 15, 2016): 1. http://dx.doi.org/10.22580/2016/iscinotej1.1.2.

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9

Blankson, Joel, Deborah Persaud, and Robert F. Siliciano. "Latent reservoirs for HIV-1." Current Opinion in Infectious Diseases 12, no. 1 (February 1999): 5–11. http://dx.doi.org/10.1097/00001432-199902000-00002.

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10

Koup, Richard A. "A new latent HIV reservoir." Nature Medicine 7, no. 4 (April 2001): 404–5. http://dx.doi.org/10.1038/86455.

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11

O'Neill, Paul. "A handle on latent HIV." Trends in Molecular Medicine 7, no. 6 (June 2001): 244. http://dx.doi.org/10.1016/s1471-4914(01)02058-5.

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12

Cary, Daniele C., Koh Fujinaga, and B. Matija Peterlin. "Euphorbia Kansui Reactivates Latent HIV." PLOS ONE 11, no. 12 (December 15, 2016): e0168027. http://dx.doi.org/10.1371/journal.pone.0168027.

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13

Hokello, Joseph, Adhikarimayum Lakhikumar Sharma, Manjari Dimri, and Mudit Tyagi. "Insights into the HIV Latency and the Role of Cytokines." Pathogens 8, no. 3 (September 4, 2019): 137. http://dx.doi.org/10.3390/pathogens8030137.

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Human immunodeficiency virus-1 (HIV-1) has the ability to infect latently at the level of individual CD4+ cells. Latent HIV-1 proviruses are transcriptionally silent and immunologically inert, but are still capable of reactivating productive lytic infection following cellular activation. These latent viruses are the main obstacle in the eradication of HIV-1, because current HIV-1 treatment regimens are ineffective against them. Normal immunological response against an antigen activates CD4+ naïve T cells. The activated CD4+ naïve T cells undergo cell cycle, resulting in further transformation and profound proliferation to form effector CD4+ T-cells. Notably, in HIV-1 infected individuals, some of the effector CD4+ T cells get infected with HIV-1. Upon fulfillment of their effector functions, almost all activated CD4+ T cells are committed to apoptosis or programmed cell death, but a miniscule fraction revert to quiescence and become resting memory CD4+ T cells to mediate a rapid immunological response against the same antigen in the future. However, due to the quiescent nature of the resting memory T cells, the integrated HIV-1 becomes transcriptionally silent and acquires a latent phenotype. Following re-exposure to the same antigen, memory cells and integrated HIV-1 are stimulated. The reactivated latent HIV provirus subsequently proceeds through its life cycle and eventually leads to the production of new viral progeny. Recently, many strategies against HIV-1 latency have been developed and some of them have even matured to the clinical level, but none can yet effectively eliminate the latent HIV reservoir, which remains a barrier to HIV-1 cure. Therefore, alternative strategies to eradicate latent HIV need to be considered. This review provides vital knowledge on HIV latency and on strategies to supplement highly active anti-retroviral therapy (HAART) with cytokine-mediated therapeutics for dislodging the latent HIV reservoirs in order to open up new avenues for curing HIV.

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Sahay, Bikash, and Ayalew Mergia. "The Potential Contribution of Caveolin 1 to HIV Latent Infection." Pathogens 9, no. 11 (October 27, 2020): 896. http://dx.doi.org/10.3390/pathogens9110896.

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Combinatorial antiretroviral therapy (cART) suppresses HIV replication to undetectable levels and has been effective in prolonging the lives of HIV infected individuals. However, cART is not capable of eradicating HIV from infected individuals mainly due to HIV’s persistence in small reservoirs of latently infected resting cells. Latent infection occurs when the HIV-1 provirus becomes transcriptionally inactive and several mechanisms that contribute to the silencing of HIV transcription have been described. Despite these advances, latent infection remains a major hurdle to cure HIV infected individuals. Therefore, there is a need for more understanding of novel mechanisms that are associated with latent infection to purge HIV from infected individuals thoroughly. Caveolin 1(Cav-1) is a multifaceted functional protein expressed in many cell types. The expression of Cav-1 in lymphocytes has been controversial. Recent evidence, however, convincingly established the expression of Cav-1 in lymphocytes. In lieu of this finding, the current review examines the potential role of Cav-1 in HIV latent infection and provides a perspective that helps uncover new insights to understand HIV latent infection.

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15

Seu, Lillian, Steffanie Sabbaj, Alexandra Duverger, Frederic Wagner, Joshua C. Anderson, Elizabeth Davies, Frank Wolschendorf, et al. "Stable Phenotypic Changes of the Host T Cells Are Essential to the Long-Term Stability of Latent HIV-1 Infection." Journal of Virology 89, no. 13 (April 15, 2015): 6656–72. http://dx.doi.org/10.1128/jvi.00571-15.

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ABSTRACTThe extreme stability of the latent HIV-1 reservoir in the CD4+memory T cell population prevents viral eradication with current antiretroviral therapy. It has been demonstrated that homeostatic T cell proliferation and clonal expansion of latently infected T cells due to viral integration into specific genes contribute to this extraordinary reservoir stability. Nevertheless, given the constant exposure of the memory T cell population to specific antigen or bystander activation, this reservoir stability seems remarkable, unless it is assumed that latent HIV-1 resides exclusively in memory T cells that recognize rare antigens. Another explanation for the stability of the reservoir could be that the latent HIV-1 reservoir is associated with an unresponsive T cell phenotype. We demonstrate here that host cells of latent HIV-1 infection events were functionally altered in ways that are consistent with the idea of an anergic, unresponsive T cell phenotype. Manipulations that induced or mimicked an anergic T cell state promoted latent HIV-1 infection. Kinome analysis data reflected this altered host cell phenotype at a system-wide level and revealed how the stable kinase activity changes networked to stabilize latent HIV-1 infection. Protein-protein interaction networks generated from kinome data could further be used to guide targeted genetic or pharmacological manipulations that alter the stability of latent HIV-1 infection. In summary, our data demonstrate that stable changes to the signal transduction and transcription factor network of latently HIV-1 infected host cells are essential to the ability of HIV-1 to establish and maintain latent HIV-1 infection status.IMPORTANCEThe extreme stability of the latent HIV-1 reservoir allows the infection to persist for the lifetime of a patient, despite completely suppressive antiretroviral therapy. This extreme reservoir stability is somewhat surprising, since the latently HIV-1 infected CD4+memory T cells that form the structural basis of the viral reservoir should be exposed to cognate antigen over time. Antigen exposure would trigger a recall response and should deplete the reservoir, likely over a relatively short period. Our data demonstrate that stable and system-wide phenotypic changes to host cells are a prerequisite for the establishment and maintenance of latent HIV-1 infection events. The changes observed are consistent with an unresponsive, anergy-like T cell phenotype of latently HIV-1 infected host cells. An anergy-like, unresponsive state of the host cells of latent HIV-1 infection events would explain the stability of the HIV-1 reservoir in the face of continuous antigen exposure.

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16

Huang, Xu-Sheng, Ren-Rong Tian, Meng-Di Ma, Rong-Hua Luo, Liu-Meng Yang, Guang-Hui Peng, Mi Zhang, Xing-Qi Dong, and Yong-Tang Zheng. "Bromodomain and Extra-Terminal Inhibitor BMS-986158 Reverses Latent HIV-1 Infection In Vitro and Ex Vivo by Increasing CDK9 Phosphorylation and Recruitment." Pharmaceuticals 15, no. 3 (March 10, 2022): 338. http://dx.doi.org/10.3390/ph15030338.

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Latent reservoir persistence remains a major obstacle for curing human immunodeficiency virus type 1 (HIV-1) infection. Thus, strategies for the elimination of latent HIV-1 are urgently needed. As a bromodomain and extra-terminal (BET) inhibitor, BMS-986158 has been used in clinical trials for advanced solid tumors and hematological malignancies. Here, we found that BMS-986158 reactivated latent HIV-1 in three types of HIV-1 latency cells in vitro, and in combination antiretroviral therapy (cART)-treated patient-derived peripheral blood mononuclear cells ex vivo, without influencing global immune cell activation. BMS-986158 reactivated latent HIV-1 by increasing phosphorylation of CDK9 at Thr186 and promoting recruitment of CDK9 and RNA polymerase II to the HIV-1 long terminal repeat in J-Lat cells. Furthermore, BMS-986158 exerted strong synergism in reactivating latent HIV-1 when combined with prostratin and vorinostat and enhanced the antiviral activity of anti-HIV-1 drugs. Finally, BMS-986158 showed antiviral activity in an HIV-1 acute infection model, possibly by arresting the cell cycle in infected cells. Thus, these results suggest that BMS-986158 is a potential candidate for AIDS/HIV-1 therapy.

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17

Sarabia, Indra, and Alberto Bosque. "HIV-1 Latency and Latency Reversal: Does Subtype Matter?" Viruses 11, no. 12 (November 28, 2019): 1104. http://dx.doi.org/10.3390/v11121104.

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Cells that are latently infected with HIV-1 preclude an HIV-1 cure, as antiretroviral therapy does not target this latent population. HIV-1 is highly genetically diverse, with over 10 subtypes and numerous recombinant forms circulating worldwide. In spite of this vast diversity, much of our understanding of latency and latency reversal is largely based on subtype B viruses. As such, most of the development of cure strategies targeting HIV-1 are solely based on subtype B. It is currently assumed that subtype does not influence the establishment or reactivation of latent viruses. However, this has not been conclusively proven one way or the other. A better understanding of the factors that influence HIV-1 latency in all viral subtypes will help develop therapeutic strategies that can be applied worldwide. Here, we review the latest literature on subtype-specific factors that affect viral replication, pathogenesis, and, most importantly, latency and its reversal.

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18

Ajayi, Bamidele David, John Omotola Ogunkoya, and Folake Olubunmi Ajayi. "Latent Tuberculosis Infection and Isoniazid Preventive Therapy among Human Immunodeficiency Virus positive adults in Southern Nigeria." Research Journal of Health Sciences 10, no. 4 (December 8, 2022): 305–18. http://dx.doi.org/10.4314/rejhs.v10i4.1.

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Aim/objectives: It was aimed to assess the prevalence of latent TB among HIV+ patients, evaluate the coverage of isoniazid preventive therapy (IPT), the continuous risk of latent tuberculosis infection, and factors associated with the presence of latent Tb in HIV+ patients. Methods: This is an analytical cross-sectional study of HIV+ patients attending the HIV clinic or admitted not previously treated for TB and did not have clinical and laboratory evidence of active TB and matched HIV-negative population attending our GOC. Data collected with a pre-tested investigator administered questionnaire included the age, sex, height and weight, medical and drug history, and relevant physical examination findings such as body temperature and respiratory rate. Active TB was excluded by history, sputum AFB Z-N staining, or GeneXpert test and chest radiography. Whole blood samples were collected from participants for QuantiFERON TB Gold Plus for quantification of Interferon Gamma Release assay (IGRA) in order to diagnose or exclude latent TB. Data were analyzed using IBM SPSS version 25.0 software at a level of significance of p < 0.05. Association between means and qualitative variables was analyzed with student-t-test and Chi-square test Results: The mean ages of the HIV+ and control groups were 42.69 ± 9.91 and 41.29 ± 9.20 years respectively with no significant statistical difference. 76(95.0%) of HIV+ patients and 74(92.5%) controls had no symptoms of TB and chronic lung disease. 18(22.5%) HIV+ patients and 2(2.5%) controls were exposed to persons with chronic cough (p=<0.001). The prevalence of latent TB among HIV+ patients was 22.50% and 10.0% among controls (p- value=0.001). 8(44.4%) out of 18 with latent TB had prior use of IPT compared with 24 (38.7%) out of 62 without latent TB (p-value =0.67). CD4 count was a significant factor associated with the presence of latent TB among HIV+ persons (p-0.03). Similarly, there was a significant association between viral load and positive IGRA (p<0.001). Conclusion: Latent TB infection remains significantly higher among HIV+ than HIV-negative patients which may account for the higher incidence of active disease amongst them. Isoniazid preventive therapy coverage was poor amongst HIV+ patients in this study.

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19

Marsden, Matthew D., and Jerome A. Zack. "Experimental Approaches for Eliminating Latent HIV." Forum on Immunopathological Diseases and Therapeutics 6, no. 1-2 (2015): 91–99. http://dx.doi.org/10.1615/forumimmundisther.2016015242.

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20

Hodel, Flavia, Marion Patxot, Tiia Snäkä, and Angela Ciuffi. "HIV-1 latent reservoir: size matters." Future Virology 11, no. 12 (December 2016): 785–94. http://dx.doi.org/10.2217/fvl-2016-0093.

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21

Uliukin, I. M. "LATENT DEPRESSION IN HIV AFFECTED WOMEN." HIV Infection and Immunosuppressive Disorders 9, no. 3 (January 1, 2017): 16–27. http://dx.doi.org/10.22328/2077-9828-2017-9-3-16-27.

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22

Cary, Daniele C., and B. Matija Peterlin. "Proteasomal Inhibition Potentiates Latent HIV Reactivation." AIDS Research and Human Retroviruses 36, no. 10 (October 1, 2020): 800–807. http://dx.doi.org/10.1089/aid.2020.0040.

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23

Zhao, Jia-Cong, and Kai Deng. "Heterogeneity of HIV-1 latent reservoirs." Chinese Medical Journal 133, no. 23 (September 15, 2020): 2867–73. http://dx.doi.org/10.1097/cm9.0000000000001085.

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24

Brower, Vicki. "Latent HIV needs second knockout punch." Nature Biotechnology 16, no. 1 (January 1998): 15. http://dx.doi.org/10.1038/nbt0198-15.

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25

Barton, K. M., B. D. Burch, N. Soriano-Sarabia, and D. M. Margolis. "Prospects for Treatment of Latent HIV." Clinical Pharmacology & Therapeutics 93, no. 1 (October 10, 2012): 46–56. http://dx.doi.org/10.1038/clpt.2012.202.

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26

Barton, Samantha. "Emptying reservoirs of latent HIV-1." Nature Reviews Drug Discovery 4, no. 11 (October 24, 2005): 886. http://dx.doi.org/10.1038/nrd1888.

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Xu, Xinfeng, Yingtong Lin, Xiaoyun Zeng, Chan Yang, Siqin Duan, Liqiong Ding, Wanzhen Lu, et al. "PARP1 Might Substitute HSF1 to Reactivate Latent HIV-1 by Binding to Heat Shock Element." Cells 11, no. 15 (July 29, 2022): 2331. http://dx.doi.org/10.3390/cells11152331.

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At present, the barrier to HIV-1 functional cure is the persistence of HIV-1 reservoirs. The “shock (reversing latency) and kill (antiretroviral therapy)” strategy sheds light on reducing or eliminating the latent reservoir of HIV-1. However, the current limits of latency-reversing agents (LRAs) are their toxicity or side effects, which limit their practicability pharmacologically and immunologically. Our previous research found that HSF1 is a key transcriptional regulatory factor in the reversion of HIV-1 latency. We then constructed the in vitro HSF1-knockout (HSF1-KO) HIV-1 latency models and found that HSF1 depletion inhibited the reactivation ability of LRAs including salubrinal, carfizomib, bortezomib, PR-957 and resveratrol, respectively. Furthermore, bortezomib/carfizomib treatment induced the increase of heat shock elements (HSEs) activity after HSF1-KO, suggesting that HSEs participated in reversing the latent HIV-1. Subsequent investigation showed that latent HIV-1-reversal by H2O2-induced DNA damage was inhibited by PARP1 inhibitors, while PARP1 was unable to down-regulate HSF1-depleted HSE activity, indicating that PARP1 could serve as a replaceable protein for HSF1 in HIV-1 latent cells. In summary, we succeeded in finding the mechanisms by which HSF1 reactivates the latent HIV-1, which also provides a theoretical basis for the further development of LRAs that specifically target HSF1.

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Barclay, Robert A., Gifty A. Mensah, Maria Cowen, Catherine DeMarino, Yuriy Kim, Daniel O. Pinto, James Erickson, and Fatah Kashanchi. "Extracellular Vesicle Activation of Latent HIV-1 Is Driven by EV-Associated c-Src and Cellular SRC-1 via the PI3K/AKT/mTOR Pathway." Viruses 12, no. 6 (June 19, 2020): 665. http://dx.doi.org/10.3390/v12060665.

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HIV-1 is a global health crisis that has infected more than 37 million people. Latent reservoirs throughout the body are a major hurdle when it comes to eradicating the virus. In our previous study, we found that exosomes, a type of extracellular vesicle (EV), from uninfected cells activate the transcription of HIV-1 in latent infected cells, regardless of combination antiretroviral therapy (cART). In this study, we investigated the specific mechanism behind the EV activation of latent HIV-1. We found that phosphorylated c-Src is present in EVs of various cell lines and has the ability to activate downstream proteins such as EGFR, initiating a signal cascade. EGFR is then able to activate the PI3K/AKT/mTOR pathway, resulting in the activation of STAT3 and SRC-1, culminating in the reversal of HIV-1 latency. This was verified by examining levels of HIV-1 TAR, genomic RNA and HIV-1 Gag p24 protein in cell lines and primary cells. We found that EVs containing c-Src rescued HIV-1 despite the presence of inhibitors, validating the importance of EV-associated c-Src in latent HIV-1 activation. Lastly, we discovered an increased recruitment of p300 and NF-κB in the nucleus of EV-treated infected cells. Collectively, our data suggest that EV-associated c-Src is able to activate latent HIV-1 via the PI3K/AKT/mTOR pathway and SRC-1/p300-driven chromatin remodeling. These findings could aid in designing new strategies to prevent the reactivation of latent HIV-1 in patients under cART.

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Warren, Joanna A., Shuntai Zhou, Yinyan Xu, Matthew Moeser, Jenn Kirchherr, Julia Sung, Nadia Roan, et al. "Quantifying Virus Escape from T Cells in the Latent HIV Reservoir." Journal of Immunology 202, no. 1_Supplement (May 1, 2019): 197.14. http://dx.doi.org/10.4049/jimmunol.202.supp.197.14.

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Abstract There is no cure for HIV, largely because HIV establishes a small but sustained pool of latently infected cells that are not cleared by antiretroviral therapy (ART). Current strategies include firstly reactivating the latent HIV reservoir and then using T cell immunotherapy to clear reactivated cells. However, pre-ART CD8 T cell escape variants have been reported in the HIV reservoir, which may limit CD8 T cell recognition and clearance of HIV-infected cells. The extent of virus escape from T cells in the latent reservoir is unclear. HIV-specific T cell responses were comprehensively mapped across the Clade B HIV proteome by IFN-g ELISpot in 25 ART-suppressed participants. In parallel, replication competent viruses derived from supernatants of autologous resting CD4 T cells following mitogenic reactivation were sequenced. Peptides spanning virus variants within reactive T cell epitopes were synthesized and examined by ELISpot for evidence of escape, defined as ≥50% difference in T cell magnitude between peptide variants. No correlations were observed between the size of the latent HIV reservoir and either HIV-specific T cell breadth (1–19 epitopes) or magnitude (156–2855 SFU/M PBMCs). T cell escape was assessed in 17 participants. 39% of reactive T cell epitopes (48/124) harbored ≥1 amino acid variants in the sequenced latent reservoir. Of those 48, 20 afforded T cell escape, providing an overall escape frequency in the reservoir of 16% (20/124). These data show that the majority of replication competent latent HIV viruses do not harbor CD8 T cell escape mutants, suggesting that immunotherapy approaches that boost CD8 T cell responses can successfully target the latent reservoir in HIV curative and or remission strategies.

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Zellweger, Jean-Pierre. "Latent Tuberculosis Infection." European Respiratory & Pulmonary Diseases 4, no. 1 (2018): 21. http://dx.doi.org/10.17925/erpd.2018.4.1.21.

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Tuberculosis (TB) is a major global public health problem and is the leading cause of death linked to a single pathogen, ranking above human immunodeficiency virus (HIV).¹ Clinically, TB has been categorised as active disease (patients who are generally symptomatic and may be infectious if pulmonary involvement is present) and latent infection (asymptomatic and not infectious, but at variable risk for progression to active TB disease). It is increasingly being recognised that latent TB infection (LTBI) reflects diverse responses to infection with Mycobacterium tuberculosis and may lead to heterogeneous clinical outcomes. In an expert interview, Jean-Pierre Zellweger discusses the latest World Health Organisation (WHO) guidelines on the management of LTBI.

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Feng, Zeming, Zhengrong Yang, Xiang Gao, Yuhua Xue, and Xiaohui Wang. "Resveratrol Promotes HIV-1 Tat Accumulation via AKT/FOXO1 Signaling Axis and Potentiates Vorinostat to Antagonize HIV-1 Latency." Current HIV Research 19, no. 3 (May 6, 2021): 238–47. http://dx.doi.org/10.2174/1570162x19666210118151249.

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Background: The latent reservoir of HIV-1 is a major barrier to achieving the eradication of HIV-1/AIDS. One strategy is termed “shock and kill”, which aims to awaken the latent HIV-1 using latency reversing agents (LRAs) to replicate and produce HIV-1 particles. Subsequently, the host cells containing HIV-1 can be recognized and eliminated by the immune response and anti-retroviral therapy. Although many LRAs have been found and tested, their clinical trials were dissatisfactory. Objective: To aim of the study was to investigate how resveratrol reactivates silent HIV-1 transcription and assess if resveratrol could be a candidate drug for the “shock” phase in “shock and kill” strategy. Method: We used established HIV-1 transcription cell models (HeLa-based NH1 and NH2 cells) and HIV-1 latent cell models (J-Lat A72 and Jurkat 2D10 cells). We performed resveratrol treatment on these cell lines and studied the mechanism of how resveratrol stimulates HIV-1 gene transcription. We also tested resveratrol’s bioactivity on primary cells isolated from HIV-1 latent infected patients. Results: Resveratrol promoted HIV-1 Tat protein levels, and resveratrol-induced Tat promotion was found to be dependent on the AKT/FOXO1 signaling axis. Resveratrol could partially dissociate P-TEFb (Positive Transcription Elongation Factor b) from 7SK snRNP (7SK small nuclear Ribonucleoprotein) and promote Tat-SEC (Super Elongation Complex) interaction. Preclinical studies showed that resveratrol potentiated Vorinostat to awaken HIV-1 latency in HIV-1 latent infected cells isolated from patients. Conclusion: We found a new mechanism of resveratrol stimulating the production of HIV-1. Resveratrol could be a promising candidate drug to eradicate HIV-1 reservoirs.

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Pinto, Carla M. A., Ana R. M. Carvalho, Dumitru Baleanu, and Hari M. Srivastava. "Efficacy of the Post-Exposure Prophylaxis and of the HIV Latent Reservoir in HIV Infection." Mathematics 7, no. 6 (June 5, 2019): 515. http://dx.doi.org/10.3390/math7060515.

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We propose a fractional order model to study the efficacy of the Post-Exposure Prophylaxis (PEP) in human immunodeficiency virus (HIV) within-host dynamics, in the presence of the HIV latent reservoir. Latent reservoirs harbor infected cells that contain a transcriptionally silent but reactivatable provirus. The latter constitutes a major difficulty to the eradication of HIV in infected patients. PEP is used as a way to prevent HIV infection after a recent possible exposure to HIV. It consists of the in-take of antiretroviral drugs for, usually, 28 days. In this study, we focus on the dosage and dosage intervals of antiretroviral therapy (ART) during PEP and in the role of the latent reservoir in HIV infected patients. We thus simulate the model for immunologically important parameters concerning the drugs and the fraction of latently infected cells. The results may add important information to clinical practice of HIV infected patients.

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Scripture-Adams, Deirdre D., David G. Brooks, Yael D. Korin, and Jerome A. Zack. "Interleukin-7 Induces Expression of Latent Human Immunodeficiency Virus Type 1 with Minimal Effects on T-Cell Phenotype." Journal of Virology 76, no. 24 (December 15, 2002): 13077–82. http://dx.doi.org/10.1128/jvi.76.24.13077-13082.2002.

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ABSTRACT Latent human immunodeficiency virus type 1 (HIV-1) persists even in patients treated with antiretroviral therapy. New treatment strategies are therefore needed to eradicate this latent viral reservoir without reducing immune cell function. We characterize the interleukin-7 (IL-7)-induced stimulation of primary human T cells and thymocytes and demonstrate, using the SCID-hu model, that IL-7 induces substantial expression of latent HIV while having minimal effects on the cell phenotype. Thus, IL-7 is a viable candidate to activate expression of latent HIV and may facilitate immune clearance of latently infected cells.

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Yazdani, Kiana, Katerina Dolguikh, Wendy Zhang, Sara Shayegi-Nik, Jessica Ly, Shaughna Cooper, Jason Trigg, et al. "Knowledge of hepatitis C and awareness of reinfection risk among people who successfully completed direct acting antiviral therapy." PLOS ONE 17, no. 3 (March 23, 2022): e0265811. http://dx.doi.org/10.1371/journal.pone.0265811.

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Background Hepatitis C virus (HCV) education may be changing following the simplification of HCV treatment and emergence of direct acting antiviral (DAA). We aimed to characterize HCV knowledge among people who recently completed DAA therapy. Methods The Per-SVR (Preservation of Sustained Virologic Response) is a prospective cohort of patients who achieved a sustained virologic response upon successful completion of DAA therapy. The per-SVR study provided the sampling frame of participants who completed a psychometrically validated 19-item HCV knowledge scale at cohort entry (n = 227). To score the questionnaire, for each correct response one point was awarded, with no point for incorrect response. We assessed mean HCV knowledge score in the overall sample and mutually exclusive populations: people who inject drug (PWID) (n = 71); people with co-occurring HIV (n = 23); PWID and co-occurring HIV (n = 29), and others (n = 104) Using a latent class analysis based on distal outcome, we identified unobserved subgroups and assessed HCV knowledge amongst them. Results Total mean (SD) percent of correct responses were 83 (11) in the overall sample; 83 (10) in PWID; 79 (12) in people with co-occurring HIV; 81 (10) in PWID and co-occurring HIV, and 84 (11) in rest of the sample Three latent groups were identified: baby boomers who ever experienced homelessness (n = 126); women sex workers who ever experienced homelessness (n = 68); men who inject drug, ever experienced homelessness and had ever diagnosis of mental health disorders (n = 18). Mean percent of correct responses were 85 (8), 82 (11), 85 (10), in latent class 1, 2, and 3, respectively. Conclusion Patients successfully treated with DAAs had a high HCV knowledge. High knowledge and awareness of reinfection among complex patient groups often facing barriers to HCV care is encouraging and emphasizes the positive outcomes of universal access to treatment.

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Jones, Bradley R., Natalie N. Kinloch, Joshua Horacsek, Bruce Ganase, Marianne Harris, P. Richard Harrigan, R. Brad Jones, et al. "Phylogenetic approach to recover integration dates of latent HIV sequences within-host." Proceedings of the National Academy of Sciences 115, no. 38 (September 5, 2018): E8958—E8967. http://dx.doi.org/10.1073/pnas.1802028115.

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Given that HIV evolution and latent reservoir establishment occur continually within-host, and that latently infected cells can persist long-term, the HIV reservoir should comprise a genetically heterogeneous archive recapitulating within-host HIV evolution. However, this has yet to be conclusively demonstrated, in part due to the challenges of reconstructing within-host reservoir establishment dynamics over long timescales. We developed a phylogenetic framework to reconstruct the integration dates of individual latent HIV lineages. The framework first involves inference and rooting of a maximum-likelihood phylogeny relating plasma HIV RNA sequences serially sampled before the initiation of suppressive antiretroviral therapy, along with putative latent sequences sampled thereafter. A linear model relating root-to-tip distances of plasma HIV RNA sequences to their sampling dates is used to convert root-to-tip distances of putative latent lineages to their establishment (integration) dates. Reconstruction of the ages of putative latent sequences sampled from chronically HIV-infected individuals up to 10 y following initiation of suppressive therapy revealed a genetically heterogeneous reservoir that recapitulated HIV’s within-host evolutionary history. Reservoir sequences were interspersed throughout multiple within-host lineages, with the oldest dating to >20 y before sampling; historic genetic bottleneck events were also recorded therein. Notably, plasma HIV RNA sequences isolated from a viremia blip in an individual receiving otherwise suppressive therapy were highly genetically diverse and spanned a 20-y age range, suggestive of spontaneous in vivo HIV reactivation from a large latently infected cell pool. Our framework for reservoir dating provides a potentially powerful addition to the HIV persistence research toolkit.

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Friedman, Eleanor E., Awal Khan, and Wayne A. Duffus. "Screening for Latent Tuberculosis Infection Among HIV-Infected Medicaid Enrollees." Public Health Reports 133, no. 4 (June 21, 2018): 413–22. http://dx.doi.org/10.1177/0033354918776639.

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Objectives: In the United States, universal screening for latent tuberculosis (TB) infection among people with HIV is recommended, but the percentage receiving screening is unknown. This study assessed screening for latent TB infection among people with HIV enrolled in Medicaid during 2006-2010. Methods: We used nationwide fee-for-service Medicaid records to identify people with HIV, measure screening for latent TB infection, and examine associated demographic, social, and clinical factors. We used logistic regression analysis to calculate odds ratios (ORs) and 95% confidence intervals (CIs). We created 2 multivariate models to prevent collinearity between variables for length of HIV infection. Results: Of 152 831 people with HIV, 26 239 (17.2%) were screened for latent TB infection. The factor most strongly associated with screening was TB exposure or suspected TB (OR = 3.78; 95% CI, 3.27-4.37). Significant demographic characteristics associated with screening included being African American (OR = 1.28; 95% CI, 1.24-1.32) or ≤20 years of age (OR = 1.35; 95% CI, 1.28-1.42). Significant clinical and social factors associated with screening included poor housing conditions, low body mass index, chemotherapy treatment, and use of certain substances (ORs ranged from 1.24 [95% CI, 1.20-1.27] to 1.47 [95% CI, 1.22-1.76]). The screening rate for latent TB infection was higher among people with newly diagnosed HIV infection than among those with established infection (OR = 1.37; 95% CI, 1.32-1.41) and among people with a longer established HIV infection than among those with shorter HIV infection (OR = 1.24; 95% CI, 1.23-1.26 for each additional year). Conclusion: Screening for latent TB infection among fee-for-service Medicaid beneficiaries with HIV was suboptimal, despite the presence of demographic, social, or clinical characteristics that should have increased the likelihood of screening. The lack of certain data in Medicaid may have resulted in an underestimation of screening.

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Nguyen, Kien, Curtis Dobrowolski, Meenakshi Shukla, Won-Kyung Cho, Benjamin Luttge, and Jonathan Karn. "Inhibition of the H3K27 demethylase UTX enhances the epigenetic silencing of HIV proviruses and induces HIV-1 DNA hypermethylation but fails to permanently block HIV reactivation." PLOS Pathogens 17, no. 10 (October 21, 2021): e1010014. http://dx.doi.org/10.1371/journal.ppat.1010014.

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One strategy for a functional cure of HIV-1 is “block and lock”, which seeks to permanently suppress the rebound of quiescent HIV-1 by epigenetic silencing. For the bivalent promoter in the HIV LTR, both histone 3 lysine 27 tri-methylation (H3K27me3) and DNA methylation are associated with viral suppression, while H3K4 tri-methylation (H3K4me3) is correlated with viral expression. However, H3K27me3 is readily reversed upon activation of T-cells through the T-cell receptor. In an attempt to suppress latent HIV-1 in a stable fashion, we knocked down the expression or inhibited the activity of UTX/KDM6A, the major H3K27 demethylase, and investigated its impact on latent HIV-1 reactivation in T cells. Inhibition of UTX dramatically enhanced H3K27me3 levels at the HIV LTR and was associated with increased DNA methylation. In latently infected cells from patients, GSK-J4, which is a potent dual inhibitor of the H3K27me3/me2-demethylases JMJD3/KDM6B and UTX/KDM6A, effectively suppressed the reactivation of latent HIV-1 and also induced DNA methylation at specific sites in the 5’LTR of latent HIV-1 by the enhanced recruitment of DNMT3A to HIV-1. Nonetheless, suppression of HIV-1 through epigenetic silencing required the continued treatment with GSK-J4 and was rapidly reversed after removal of the drug. DNA methylation was also rapidly lost after removal of drug, suggesting active and rapid DNA-demethylation of the HIV LTR. Thus, induction of epigenetic silencing by histone and DNA methylation appears to be insufficient to permanently silence HIV-1 proviral transcription.

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Huang, Huachao, Weili Kong, Maxime Jean, Guillaume Fiches, Dawei Zhou, Tsuyoshi Hayashi, Jianwen Que, Netty Santoso, and Jian Zhu. "A CRISPR/Cas9 screen identifies the histone demethylase MINA53 as a novel HIV-1 latency-promoting gene (LPG)." Nucleic Acids Research 47, no. 14 (June 5, 2019): 7333–47. http://dx.doi.org/10.1093/nar/gkz493.

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AbstractAlthough combination antiretroviral therapy is potent to block active replication of HIV-1 in AIDS patients, HIV-1 persists as transcriptionally inactive proviruses in infected cells. These HIV-1 latent reservoirs remain a major obstacle for clearance of HIV-1. Investigation of host factors regulating HIV-1 latency is critical for developing novel antiretroviral reagents to eliminate HIV-1 latent reservoirs. From our recently accomplished CRISPR/Cas9 sgRNA screens, we identified that the histone demethylase, MINA53, is potentially a novel HIV-1 latency-promoting gene (LPG). We next validated MINA53’s function in maintenance of HIV-1 latency by depleting MINA53 using the alternative RNAi approach. We further identified that in vitro MINA53 preferentially demethylates the histone substrate, H3K36me3 and that in cells MINA53 depletion by RNAi also increases the local level of H3K36me3 at LTR. The effort to map the downstream effectors unraveled that H3K36me3 has the cross-talk with another epigenetic mark H4K16ac, mediated by KAT8 that recognizes the methylated H3K36 and acetylated H4K16. Removing the MINA53-mediated latency mechanisms could benefit the reversal of post-integrated latent HIV-1 proviruses for purging of reservoir cells. We further demonstrated that a pan jumonji histone demethylase inhibitor, JIB-04, inhibits MINA53-mediated demethylation of H3K36me3, and JIB-04 synergizes with other latency-reversing agents (LRAs) to reactivate latent HIV-1.

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Murray, John M. "Dynamics of latent HIV under clonal expansion." PLOS Pathogens 17, no. 12 (December 20, 2021): e1010165. http://dx.doi.org/10.1371/journal.ppat.1010165.

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The HIV latent reservoir exhibits slow decay on antiretroviral therapy (ART), impacted by homeostatic proliferation and activation. How these processes contribute to the total dynamic while also producing the observed profile of sampled latent clone sizes is unclear. An agent-based model was developed that tracks individual latent clones, incorporating homeostatic proliferation of cells and activation of clones. The model was calibrated to produce observed latent reservoir dynamics as well as observed clonal size profiles. Simulations were compared to previously published latent HIV integration data from 5 adults and 3 children. The model simulations reproduced reservoir dynamics as well as generating residual plasma viremia levels (pVL) consistent with observations on ART. Over 382 Latin Hypercube Sample simulations, the median latent reservoir grew by only 0.3 log10 over the 10 years prior to ART initiation, after which time it decreased with a half-life of 15 years, despite number of clones decreasing at a faster rate. Activation produced a maximum size of genetically intact clones of around one million cells. The individual simulation that best reproduced the sampled clone profile, produced a reservoir that decayed with a 13.9 year half-life and where pVL, produced mainly from proliferation, decayed with a half-life of 10.8 years. These slow decay rates were achieved with mean cell life-spans of only 14.2 months, due to expansion of the reservoir through proliferation and activation. Although the reservoir decayed on ART, a number of clones increased in size more than 4,000-fold. While small sampled clones may have expanded through proliferation, the large sizes exclusively arose from activation. Simulations where homeostatic proliferation contributed more to pVL than activation, produced pVL that was less variable over time and exhibited fewer viral blips. While homeostatic proliferation adds to the latent reservoir, activation can both add and remove latent cells. Latent activation can produce large clones, where these may have been seeded much earlier than when first sampled. Elimination of the reservoir is complicated by expanding clones whose dynamic differ considerably to that of the entire reservoir.

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Côté, Pierre, Jean-Guy Baril, Marie-Nicole Hébert, Marina Klein, Richard Lalonde, Marc Poliquin, Danielle Rouleau, et al. "Management and Treatment of Hepatitis C Virus in Patients with HIV and Hepatitis C Virus Coinfection: A Practical Guide for Health Care Professionals." Canadian Journal of Infectious Diseases and Medical Microbiology 18, no. 5 (2007): 293–303. http://dx.doi.org/10.1155/2007/631054.

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Concomitant HIV and hepatitis C virus (HCV) is a common yet complex coinfection. The present document is a practical guide for treating HCV infection in people coinfected with HIV. Effective antiretroviral therapies have prolonged survival rates for HIV-infected people over the past decade, which have made latent complications of HCV major causes of morbidity and mortality in these patients. Advances in the treatment of HCV (eg, combined pegylated interferon and ribavirin) offer the possibility of eradicating HCV infection in coinfected persons. The treatment of HCV must be considered in all cases. Intensive management of the adverse effects of HCV treatment is one of the factors for the success of these therapies. HCV eradication is predicted to decrease the mortality associated with coinfection and reduce the toxicity of HIV treatment.

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Contreras, Xavier, Koen Bartholomeeusen, and B. Matija Peterlin. "Strategies and approaches to purge the latent reservoir of HIV." HIV Therapy 4, no. 1 (January 2010): 55–63. http://dx.doi.org/10.2217/hiv.09.50.

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Korin, Yael D., David G. Brooks, Stephen Brown, Andrew Korotzer, and Jerome A. Zack. "Effects of Prostratin on T-Cell Activation and Human Immunodeficiency Virus Latency." Journal of Virology 76, no. 16 (August 15, 2002): 8118–23. http://dx.doi.org/10.1128/jvi.76.16.8118-8123.2002.

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ABSTRACT Human immunodeficiency virus (HIV) replication is linked to cellular gene transcription and requires target cell activation. The latent reservoir of HIV-1 in quiescent T cells is thought to be a major obstacle to clearance of infection by highly active antiretroviral therapy (HAART). Thus, identification of agents that can induce expression of latent virus may, in the presence of HAART, allow elimination of the infected cells by the immune response. We previously used the SCID-hu (Thy/Liv) mouse model to establish that activation-inducible HIV can be generated at high frequency during thymopoiesis. Latently infected mature thymocytes can be exported into the periphery, providing an efficient primary cell model to determine cellular activation signals that induce renewed expression of latent virus. Here we characterized the effects of prostratin, a non-tumor-promoting phorbol ester, on primary human peripheral blood lymphocytes (PBLs) and assessed its ability to reactivate latent HIV infection from thymocytes and PBLs in the SCID-hu (Thy/Liv) model. Prostratin stimulation alone did not induce proliferation of quiescent PBLs; however, it could provide a secondary signal in the context of T-cell receptor stimulation or a primary activation signal in the presence of CD28 stimulation to induce T-cell proliferation. While prostratin alone was not sufficient to allow de novo HIV infection, it efficiently reactivated HIV expression from latently infected cells generated in the SCID-hu mouse. Our data indicate that prostratin alone is able to specifically reactivate latent virus in the absence of cellular proliferation, making it an attractive candidate for further study as an adjunctive therapy for the elimination of the latent HIV reservoir.

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Packard, Thomas Alexander, Eytan Herzig, Xiaoyu Luo, Johanne H. Egedal, Zachary W. Grimmett, Kim J. Hasenkrug, Nadia Roan, and Warner C. Greene. "HIV-induced production of CCL2 may promote rapid seeding of the latent HIV reservoir." Journal of Immunology 202, no. 1_Supplement (May 1, 2019): 197.2. http://dx.doi.org/10.4049/jimmunol.202.supp.197.2.

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Abstract Seeding of the latent HIV reservoir occurs quickly within hours to a few days after initial viral infection. It is the persistence of virus within this reservoir that thwarts an HIV cure and necessitates life-long antiretroviral therapy (ART). Central memory CD4 T cells harboring latent HIV proviruses form a major part of this reservoir. How the virus establishes latency so rapidly within this subset of CD4 T cells remains unknown. We find that HIV infection leads to rapid production of the CCL2 chemokine in human lymphoid CD4 T cells. Cas9RNP-mediated depletion of IFI16 and STING genes significantly reduces production of CCL2 occurring in response to HIV. IFI16 was previously implicated as the key sensor triggering CD4 T cell pyroptosis. Thus, infection may also stimulate a second pathway of IFI16-mediated signaling involving STING culminating in CCL2 production. CCL2 functions a potent chemoattractant for cells expressing CCR2. Lymphoid CCR2+ CD4 T cells express the CCR5 co-receptor for HIV and markers of central memory. Additionally, these cells express many markers previously associated with the latent HIV reservoir. CCR2+ CD4 T cells are highly permissive to latent and productive infection by both R5 and X4-tropic viruses. When CCR2+ CD4 T cells are purified from HIV-infected individuals on suppressive ART, these cells are enriched up to 75-fold for HIV proviral DNA compared to naïve cells (n=10, p=0.0078). Together, our findings support a model where HIV infection triggers the production of CCL2, leading to directed recruitment and infection of CCR2+ CD4 central memory T cells. Thus, HIV hijacks a component of the innate immune response to rapidly recruit precisely those target cells that ensure its long term persistence.

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Castro-Gonzalez, Sergio, Marta Colomer-Lluch, and Ruth Serra-Moreno. "Barriers for HIV Cure: The Latent Reservoir." AIDS Research and Human Retroviruses 34, no. 9 (September 2018): 739–59. http://dx.doi.org/10.1089/aid.2018.0118.

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McCORMACK, J. G., and L. HILEY. "Neurological features of early and latent HIV." Australian and New Zealand Journal of Medicine 20, no. 4 (August 1990): 630. http://dx.doi.org/10.1111/j.1445-5994.1990.tb01332.x.

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Kent, Stephen J., and Miles P. Davenport. "Tentative first steps to eradicate latent HIV." Lancet HIV 1, no. 1 (October 2014): e2-e3. http://dx.doi.org/10.1016/s2352-3018(14)70015-3.

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Lister, RK, M. Youle, DR Nair, AF Winder, and MHA Rustin. "Latent dysbetalipoproteinaemia precipitated by HIV-protease inhibitors." Lancet 353, no. 9165 (May 1999): 1678. http://dx.doi.org/10.1016/s0140-6736(99)01449-x.

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Deruaz, Maud, and Andrew M. Tager. "Humanized mouse models of latent HIV infection." Current Opinion in Virology 25 (August 2017): 97–104. http://dx.doi.org/10.1016/j.coviro.2017.07.027.

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Jakobsen, J., T. Smith, J. Gaub, S. Helweg-Larsen, and W. Trojaborg. "Progressive neurological dysfunction during latent HIV infection." British Medical Journal 299, no. 6693 (July 22, 1989): 225–28. http://dx.doi.org/10.1136/bmj.299.6693.225.

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Kalams, Spyros A. "Latent Infection of Cells in HIV Disease." JAMA 279, no. 10 (March 11, 1998): 807. http://dx.doi.org/10.1001/jama.279.10.807.

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