Work

Long-term persistence of HIV-infected cell clones in early treated children

Year: 2019

Type: article

Abstract: Journal of Virus Eradication 2019; 5 (Supplement 3): 1-58 28 aligned and subjected to phylogenetic and population genetic analyses; Drug resistance mutations were identified using Stanford Database.Results: The study participant is a white male HIV infected with IIIB laboratory strain of HIV, which has a stop codon in the second coding exon of tat, in 1985 via occupational exposure.He had no symptoms of acute HIV infection, but seroconverted and experienced progressive CD4 lymphopenia.He participated in a therapeutic gp160 vaccine study and CD4 cell numbers declined 156 cells/μl by 1996.He initiated antiretroviral (ARV) therapy with AZT+3TC and had increases in CD4 >350 cells/μl.When viral RNA testing was available, HIV RNA levels were initially <500 c/ml (limit of detection) but rebounded to 800 c/ml after 1 y of AZT+3TC with the emergence of M184V.Subsequent therapy was characterized by low level viremia and compromised by severe ARV adverse effects; he underwent intermittent ARV therapy from 2002-2008, and CD4 declined to 200 cells/μl.In 2010 he initiated Tenofovir DF+FTC+Efavirenz and had HIV viremia suppressed until the present.Analysis of pre-therapy plasma derived HIV RNA 11 years after infection revealed HIV remained highly related to IIIB with only 4-11 nt changes from IIIB among all pretherapy variants.Populations had limited genetic diversity (average pairwise difference 0.5% after 11 years of untreated infection).Genetic diversity accumulated slowly from 1997-2010 but remained <1 % even after >20 years of infection.Conclusions: Laboratory adapted, X4 tropic HIV-IIIB causes AIDS in vivo.Viral populations remained highly similar to the founder virus.Relatively slow change in virus diversity over time indicates the HIV reservoir was formed from a large and uniform population that persisted for years.

Source: Journal of Virus Eradication

DOI: 10.1016/s2055-6640(20)30146-1