Human Immunodeficiency Virus (HIV) Latency: The Major Hurdle in HIV Eradication

Tyagi, Mudit; Bukrinsky, Michael

doi:10.2119/molmed.2012.00194

Cited by 63 publications

(74 citation statements)

References 235 publications

(209 reference statements)

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“…Although highly active antiretroviral therapy (HAART) suppresses the HIV-1 plasma RNA load in patients to undetectable levels, latent HIV-1 infection remains in long-lived quiescent memory CD4 þ T cells, which form a reservoir established early during infection and play a role in the steady source of infectious viral particles [3,4]. Therefore, latently infected memory T cells have been considered a major hurdle in eradicating HIV infections [5]. Understanding the biological characteristics of this latent reservoir is important to develop a strategy for the elimination of these infected cells.…”

Section: Introductionmentioning

confidence: 99%

Impaired IL-2 expression in latent HIV-1 infection

Shin

Yoon

Lim

et al. 2015

Biochemical and Biophysical Research Communications

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Section: Introductionmentioning

confidence: 99%

Impaired IL-2 expression in latent HIV-1 infection

Shin

Yoon

Lim

et al. 2015

Biochemical and Biophysical Research Communications

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“…Different vaccine strategies have been devised to generate specific cellular or humoral responses, or combinations thereof, in order to prevent viral acquisition or disease progression. HIV cellular tropism, rapid escape mutations, and viral latency are major prevention and treatment hurdles (3)(4)(5)(6). Here we used transcriptional profiling of host responses to vaccination and subsequent repeated challenges to further understand the protective effects of a novel vaccination strategy based on the use of the endoplasmic reticulum resident chaperone gp96 (7).…”

mentioning

confidence: 99%

Multiple Low-Dose Challenges in a Rhesus Macaque AIDS Vaccine Trial Result in an Evolving Host Response That Affects Protective Outcome

Selinger

Štrbo

Gonzalez

et al. 2014

Clin. Vaccine Immunol.

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dUsing whole-blood transcriptional profiling, we investigated differences in the host response to vaccination and challenge in a rhesus macaque AIDS vaccine trial. Samples were collected from animals prior to and after vaccination with live, irradiated vaccine cells secreting the modified endoplasmic reticulum chaperone gp96-Ig loaded with simian immunodeficiency virus (SIV) peptides, either alone or in combination with a SIV-gp120 protein boost. Additional samples were collected following multiple low-dose rectal challenges with SIV mac251 . Animals in the boosted group had a 73% reduced risk of infection. Surprisingly, few changes in gene expression were observed during the vaccination phase. Focusing on postchallenge comparisons, in particular for protected animals, we identified a host response signature of protection comprised of strong interferon signaling after the first challenge, which then largely abated after further challenges. We also identified a host response signature, comprised of early macrophage-mediated inflammatory responses, in animals with undetectable viral loads 5 days after the first challenge but with unusually high viral titers after subsequent challenges. Statistical analysis showed that prime-boost vaccination significantly lowered the probability of infection in a time-consistent manner throughout several challenges. Given that humoral responses in the prime-boost group were highly significant prechallenge correlates of protection, the strong innate signaling after the first challenge suggests that interferon signaling may enhance vaccine-induced antibody responses and is an important contributor to protection from infection during repeated low-dose exposure to SIV.

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“…We have demonstrated that CBF-1-induced repressive chromatin structures play an important role in restricting HIV transcription and promote HIV latency in primary CD4+ T cells [105]. The role of repressive epigenetic modifications in restricting HIV transcription during latency is quite evident due to the fact that their removal or inhibition leads to the reactivation of latent proviruses [90, 91, 144, 176–178]. …”

Section: Role Of Epigenetics In Controlling Hiv Transcription and Latmentioning

confidence: 99%

The effects of cocaine on HIV transcription

et al. 2015

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Illicit drug users are a high risk population for infection with the Human Immunodeficiency Virus (HIV). A strong correlation exists between prohibited drugs use and an increase rate of HIV transmission. Cocaine stands out as one of the most frequently abused illicit drugs and its use is correlated with HIV infection and disease progression. The central nervous system (CNS) is a common target for both drugs of abuse and HIV, and cocaine intake further accelerates neuronal injury in HIV patients. Although the high incidence of HIV infection in illicit drug abusers is primarily due to high risk activities such as needle sharing and unprotected sex, several studies have demonstrated that cocaine enhances the rate of HIV gene expression and replication by activating various signal transduction pathways and downstream transcription factors. In order to generate mature HIV genomic transcript, HIV gene expression has to pass through both the initiation and elongation phases of transcription, which requires discrete transcription factors. In this review, we will provide a detailed analysis of the molecular mechanisms that regulate HIV transcription and discuss how cocaine modulates those mechanisms to upregulate HIV transcription and eventually HIV replication.

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Human Immunodeficiency Virus (HIV) Latency: The Major Hurdle in HIV Eradication

Cited by 63 publications

References 235 publications

Impaired IL-2 expression in latent HIV-1 infection

Impaired IL-2 expression in latent HIV-1 infection

Multiple Low-Dose Challenges in a Rhesus Macaque AIDS Vaccine Trial Result in an Evolving Host Response That Affects Protective Outcome

The effects of cocaine on HIV transcription

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