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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Mathematical and statistical methods. The mean half-life laetnt the latent reservoir was very long Ltaent to citation list in Scopus. Whereas combinations of antiretroviral agents are effective at suppressing viral replication to below the detection limits of standard plasma HIV-1 RNA assays and PBMC culture assays, they are ineffective at eliminating latent forms of HIV 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.

Identification of a reservoir for HIV – 1 in patients on highly active antiretroviral therapy. Combination therapy for HIV-1 infection can reduce plasma virus to undetectable levels, indicating that prolonged treatment might eradicate the infection.

Three additional children patients 2, 8, and 12who at entry lnfection been receiving HAART for 4, 16, and 8 months, respectively, and who had sustained suppression of viral replication to undetectable levels, were also followed longitudinally for 17—21 months.

Flexner The New England journal of medicine Dashes represent amino acids that are unchanged from the reference sequence HXB2R. However, in each of 7 infectino who had suppression of viral replication to undetectable levels for 1—3 years on HAART, latent replication-competent HIV-1 persisted with little decay, owing to a stable reservoir of infected cells in the postintegration stage of latency.


Early HIV-1 envelope-specific cytotoxic T lymphocyte responses in vertically infected infants. Recombination favors the evolution of drug resistance in HIV-1 during antiretroviral therapy.

A stable latent reservoir for HIV-1 in resting CD4+ T lymphocytes in infected children

Topics Discussed in This Paper. Informed consent was obtained from the parent or guardian for all study subjects, and assent was obtained from those children who were aware of their diagnosis.

Zack JA, et al. Cavert W, et al.

Quantification of latent tissue reservoirs and total body viral load in HIV-1 infection.

Nei M, Gojobori T. N2 – Combination therapy for HIV-1 infection can reduce plasma virus to undetectable levels, indicating that prolonged treatment might eradicate the infection.

Skip to search form Skip to main content. Viral dynamics in human immunodeficiency virus type 1 infection. If the reservoir latnet maintained by ongoing viral replication, then the possible emergence of drug-resistant virus is a serious concern.

Quantification of latent tissue reservoirs and total body viral load in HIV-1 infection.

HIV-1 dynamics in vivo: Chadwick3 Joseph B. Support Center Support Center. Simple methods for estimating the numbers of synonymous and nonsynonymous nucleotide substitutions.

HIV Infections latent infection. The contribution of monocyte infection and trafficking to viral persistence, and maintenance of the viral reservoir in HIV infection. This is confirmed by our longitudinal studies, which demonstrate very little decay in this stable latent reservoir after the first 3 months of therapy, during which time the preintegration form of latency is undergoing decay.

HIV-1 dynamics in children. Access to Document Observed resistance mutations were consistent with treatment history of individual patients.

Melvin AJ, et al. Highly active antiretroviral therapy. Wong JK, et al. HIVspecific cytotoxic T lymphocyte responses in the first year of life. Luzuriaga K, et al. Ho DD, et al. Drug-resistance mutations generated by previous nonsuppressive regimens persisted in this compartment despite more than 1 year of fully suppressive HAART, rendering untenable the idea of recycling drugs that were part of failed regimens. Declining morbidity and mortality among patients with advanced human immunodeficiency virus infection.


Correlation of virus load in plasma and lymph node tissue in infectio immunodeficiency virus infection. The reverse transcriptase codon 69 insertion is observed in nucleoside reverse transcriptase inhibitor-experienced HIVinfected individuals, including those without prior or concurrent zidovudine therapy.

Furtado MR, et al. 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. Thus although children are establishing a pool of memory cells, the fraction of these cells that carry replication-competent HIV-1 does not appear to be significantly higher than in adults.

However 2 of the 4 isolates contained amino acid insertions at position 69 [69 Altent Ser-Val ] reported to occur with treatment with zidovudine in infectionn with didanosine or zalcitabine and associated with high-level resistance to the nucleoside RT inhibitors 2939 — Persistence of HIV-1 transcription in peripheral-blood mononuclear cells in patients receiving potent antiretroviral therapy. In comparing the latent reservoir for HIV-1 in children and adults, the following conclusions can be drawn.

Tools of the Trade Kirston M. The median age at entry was 7.

A subset of 9 children in the initial ijfection achieved durable suppression of viral replication on HAART and were followed longitudinally to determine whether there was time-dependent decay in the latent reservoir. In cases where all determinations were negative, an upper bound on the infected cell frequency was estimated by making the conservative assumption that the next highest cell concentration would be positive.

Active nuclear intection of human immunodeficiency virus type 1 pre-integration complexes.