Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2017 Apr 26;2(2):e00138-17.
doi: 10.1128/mSphere.00138-17. eCollection 2017 Mar-Apr.

Toward a Cure: Does Host Immunity Play a Role?

Affiliations

Toward a Cure: Does Host Immunity Play a Role?

Jielin Zhang et al. mSphere. .

Abstract

Three decades of research on human immunodeficiency virus (HIV) and AIDS reveal that the human body has developed through evolution a genome immune system embodying epigenetic regulation against pathogenic nucleic acid invasion. In HIV infection, this epigenetic regulation plays a cardinal role in HIV RNA production that silences HIV transcription at a molecular (RNA) level, controls viral load at a cellular (biological) level, and governs the viremic stage of AIDS at the clinical (patient) level. Even though the human genome is largely similar among humans and HIV is a single viral species, human hosts show significant differences in viral RNA levels, ranging from cell to organ to individual and expressed as elite controllers, posttreatment controllers, and patients with AIDS. These are signature biomarkers of typical epigenetic regulation whose importance has been shunted aside by interpreting all of AIDS pathogenesis by the known properties of innate and adaptive immunity. We propose that harnessing the host genome immune system, defined as epigenetic immunity, against HIV infection will lead toward a cure.

Keywords: cure; epigenetic immunity; epigenetics; host immunity; human immunodeficiency virus.

PubMed Disclaimer

Figures

FIG 1
FIG 1
Three core factors of epigenetic immunity—the host genome’s immunity. The host protects its DNA from foreign nucleic acid invasion via an epigenetic mechanism, which consists of DNA methylation, histone acetylation/methylation, and noncoding RNA (ncRNA) activity. Each works independently but cohesively with the other two, protecting the structure and function of the host genome, ranging from heterochromatin, euchromatin, up to RNA transcription and silencing.
FIG 2
FIG 2
HERVs are close relatives of HIV, many of which have the defective genomes, and are kept silenced permanently in the human genome via epigenetic regulation for generations without causing harm.

Similar articles

Cited by

References

    1. Knipe DM, Howley PM (ed). 2013. Fields virology, 6th ed, p 1424–1473. Lippincott Williams & Wilkins, Philadelphia, PA.
    1. Ho DD, Neumann AU, Perelson AS, Chen W, Leonard JM, Markowitz M. 1995. Rapid turnover of plasma virions and CD4 lymphocytes in HIV-1 infection. Nature 373:123–126. doi:10.1038/373123a0. - DOI - PubMed
    1. Finzi D, Hermankova M, Pierson T, Carruth LM, Buck C, Chaisson RE, Quinn TC, Chadwick K, Margolick J, Brookmeyer R, Gallant J, Markowitz M, Ho DD, Richman DD, Siliciano RF. 1997. Identification of a reservoir for HIV-1 in patients on highly active antiretroviral therapy. Science 278:1295–1300. doi:10.1126/science.278.5341.1295. - DOI - PubMed
    1. von Laer D, Hufert FT, Fenner TE, Schwander S, Dietrich M, Schmitz H, Kern P. 1990. CD34+ hematopoietic progenitor cells are not a major reservoir of the human immunodeficiency virus. Blood 76:1281–1286. - PubMed
    1. Zhang J, Scadden DT, Crumpacker CS. 2007. Primitive hematopoietic cells resist HIV-1 infection via p21Waf1/Cip1/Sdi1. J Clin Invest 117:473–481. doi:10.1172/JCI28971. - DOI - PMC - PubMed

LinkOut - more resources