Latent infection of CD4+ T cells provides a mechanism for lifelong persistence of HIV-1, even in patients on effective combination therapy. Diana Finzi, Joel N. Combination therapy for HIV-1 infection can reduce plasma virus to Thus, latent infection of resting CD4+ T cells provides a mechanism for lifelong persistence Diana Finzi, Joel Blankson, +14 authors Robert F. Siliciano; Published in. Due to the importance of the latent reservoir in maintaining infection despite .. the long-term persistence of latent virus in HIV-infected individuals Finzi et al.
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Furtado MR, et al.
If the latent reservoir consists of only 1 x cells, eradication could take as long as ifection years. Access to Document The culture assay used to detect latent HIV-1 can detect cells in the preintegration state of latency and cells in the more stable postintegration state of latency. A fiinzithere are several reasons to believe that the dynamics of the latent reservoir might be different in children with perinatally acquired HIV-1 infection than in adults.
Presence of an inducible HIV-1 latent reservoir during highly active antiretroviral therapy. Hertogs K, et al. Introduction The success of combination therapy for the treatment of HIV-1 infection has resulted in a focus on sources of persistent HIV-1 in treated individuals.
The median age at entry was 7. The mean half-life of the latent reservoir was very long The zidovudine-sensitive viruses may have entered the reservoir 6 years earlier, before the initiation of zidovudine therapy, whereas the dinzi virus may have entered the reservoir 3—6 years earlier during the period of nonsuppressive therapy.
A stable latent reservoir for HIV-1 in resting CD4+ T lymphocytes in infected children
Two children had received no antiretroviral therapy at entry. Interestingly, patient 12, who was treated previously with zidovudine and didanosine and subsequently received onfection therapy with stavudine and ritonavir for 30 months, has had intermittent levels of plasma HIV-1 RNA between 30 to 50 copies over a 2-year period. A jnfection dramatic illustration of the stability of the latent reservoir is provided by the case of the child who has had the longest duration 37 months of suppression of viral replication with HAART patient 8.
Analysis of the viral isolates cultured from this compartment in a group of children who were pretreated with nonsuppressive antiretroviral regimens showed the persistence, for up to 2 years, of drug-resistant substitutions selected by previous nonsuppressive antiretroviral therapies. Patient fonzi was started on combination therapy with ritonavir 19 months before the first analysis.
The fact that in most children on HAART who have undetectable plasma virus the frequency of latently infected cells is in the range of 0.
National Center for Biotechnology InformationU. Highly active antiretroviral therapy. These results demonstrate persistence of latent HIV-1 near the limit of detection, with possible slow decay. This article has been cited by other articles in PMC.
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Mutations in retroviral genes associated with drug resistance. Quiescent T lymphocytes as an inducible virus reservoir in HIV-1 infection. Thus, in this patient who had clearly developed zidovudine-resistant virus and who is still on zidovudine, both zidovudine-sensitive virus and zidovudine-resistant virus can be found in the latent reservoir. The preintegration form of HIV-1 latency is relatively unstable, with an estimated half-life as short as 6 days J.
Blanks represent codons not determined. Recovery of replication-competent HIV despite prolonged suppression of plasma viremia. The reverse transcriptase codon 69 insertion is observed in nucleoside reverse transcriptase inhibitor-experienced HIVinfected inffection, including those without prior or concurrent zidovudine therapy.
The precise mechanisms involved in the generation of this latent reservoir are unknown; the occasional reversion of HIV-1—infected, activated T lymphocytes to a resting memory state with integrated HIV-1 is one plausible mechanism.
Positions in protease at which polymorphisms occur are shown in black type.