Next Article in Journal
Molecular Detection of Spotted-Fever Group Rickettsiae in Ticks Collected from Domestic and Wild Animals in Corsica, France
Previous Article in Journal
Spectroscopic Characterization of Bovine, Avian and Johnin Purified Protein Derivative (PPD) with High-Throughput Fourier Transform InfraRed-Based Method
Open AccessReview

Insights into the HIV Latency and the Role of Cytokines

Department of Basic Science, Kampala International University-Western Campus, Faculty of Science and Technology, Bushenyi, Uganda
Center for Translational Medicine, Thomas Jefferson University, 1020 Locust Street, Philadelphia, PA 19107, USA
Department of Biochemistry and Molecular Medicine, The George Washington University, Washington, DC 20037, USA
Author to whom correspondence should be addressed.
Pathogens 2019, 8(3), 137;
Received: 6 August 2019 / Revised: 24 August 2019 / Accepted: 1 September 2019 / Published: 4 September 2019
(This article belongs to the Section Human Pathogens)
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. View Full-Text
Keywords: HIV-1; latency; eradication; transforming growth factor-beta (TGF-β); resting memory CD4+ T-cells HIV-1; latency; eradication; transforming growth factor-beta (TGF-β); resting memory CD4+ T-cells
Show Figures

Figure 1

MDPI and ACS Style

Hokello, J.; Sharma, A.L.; Dimri, M.; Tyagi, M. Insights into the HIV Latency and the Role of Cytokines. Pathogens 2019, 8, 137.

Show more citation formats Show less citations formats
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map by Country/Region

Back to TopTop