FINZI INFECTION LATENT PDF

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

This child was treated with nonsuppressive antiretroviral regimens consisting of zidovudine, lamivudine, didanosine, and zalcitabine for 3.

Highly active antiretroviral therapy. Deficient human immunodeficiency virus type 1-specific cytotoxic T cell responses in vertically infected children. Viral load and disease progression in infants infected with human immunodeficiency virus type 1.

Recovery of replication-competent HIV despite prolonged suppression of plasma viremia. Mofenson LM, et al.

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We measured the decay rate of this latent reservoir in 34 treated adults whose plasma virus levels were undetectable. 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. Flexner The New England journal of medicine How to Define the Latent Reservoir: National Center for Biotechnology InformationU.

However, in each of 7 children 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. Topics Discussed in This Paper. 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.

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Tools of the Trade Kirston M. We measured the decay rate of this latent reservoir in 34 treated adults whose plasma virus levels were undetectable. Abstract Combination therapy for HIV-1 infection can reduce plasma virus to undetectable levels, indicating that prolonged treatment might eradicate the infection.

Link to publication in Scopus. In the incection case, the composition of the latent reservoir should not change on therapy and should reflect the virologic status before HAART. In vivo fate of HIVinfected T cells: A subset of 9 children in the initial cohort achieved durable suppression of viral replication on HAART and were followed longitudinally to determine whether there was time-dependent decay in the latent reservoir.

These results therefore establish the existence of this cellular reservoir in children. Zhang L, et al.

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

Quiescent T lymphocytes as an inducible virus reservoir in HIV-1 infection. 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. N2 – Combination therapy for HIV-1 infection can reduce plasma virus to undetectable levels, indicating that prolonged treatment might eradicate the infection. Infecfion of response in lymphoid tissues to antiretroviral therapy of HIV-1 infection.

From This Infecyion Figures, tables, and topics from this paper. Furtado MR, et al. The positions of the primers are numbered according to the pol gene of the HXB2R isolate http: Maintaining the integrity of human immunodeficiency virus sequence databases. Received Oct 30; Accepted Feb MetcalfDouglas J. Showing of extracted citations. CrandallDavid Posada Infevtion, genetics and evolution: Larder BA, et al.

The zidovudine-sensitive viruses may have entered the reservoir 6 years earlier, before the initiation of zidovudine therapy, whereas the zidovudine-resistant virus may have entered the reservoir 3—6 years earlier during the period of nonsuppressive therapy.

Studies of the kinetics of the free virus turnover in the plasma of HIV-1—infected adults and children who are treated with highly active antiretroviral therapy HAART have shown similar decay patterns. In this child, none of the 4 HIV-1 infdction cultured after 30 months of suppressive therapy with ritonavir and stavudine had genotypic substitutions in the protease gene that confer resistance to ritonavir.

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Los Alamos National Laboratory. Melvin AJ, et al. Included in this group were 6 children patients 7, 10, 11, 14, 15, and 21 who fini started on HAART and followed longitudinally.

Patient 8 was started on combination therapy with ritonavir 19 months before the first analysis. 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 Please review our privacy policy.

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. Support Center Support Center. Luzuriaga K, et al.

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

A second, slower phase decay in plasma HIV-1 RNA becomes apparent several weeks after the initiation of HAART and most likely reflects the turnover of compartments with longer half-lives, such as infected macrophages 10 Revised classification system for human immunodeficiency virus in children less than 13 years of age.

Thus although children are establishing a pool of memory cells, the fraction infectoon these cells that carry replication-competent HIV-1 does not appear to be significantly higher than in adults. This article has been cited by other articles in PMC.

Recombination favors the evolution of drug resistance in HIV-1 during antiretroviral therapy.