Efficient inhibition of both syncytium-inducing and non-syncytium-inducing wild-type HIV-1 by lamivudine in vivo

Wout, Angélique B. van‘t; Ran, Leonie; Nijhuis, Monique; Tijnagel, Jolanda M.G.H.; Groot, Tom de; Leeuwen, Remko van; Boucher, Charles A.; Schuitemaker, Hanneke; Schuurman, Rob

doi:10.1097/00002030-199810000-00009

Cited by 7 publications

(5 citation statements)

References 42 publications

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“…This might be explained by the fact that CCR5-expressing activated memory T cells demonstate a high efficiency in the activation of reverse transcriptase inhibitors 34 – 36 . Some nucleoside reverse-transcriptase inhibitors, like 3TC, are activated equally in both CCR5 and CXCR4 of target cells, and drugs do not require activation, such as the protease inhibitor ritonavir, show equal activity against both CCR5- and CXCR4-specific variants 28 , 36 , 37 .…”

Section: Discussionmentioning

confidence: 99%

Effects of HIV-1 genotype on baseline CD4+ cell count and mortality before and after antiretroviral therapy

Cao

Chen

et al. 2020

Sci Rep

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To assess whether human immunodeficiency virus type 1 (HIV-1) genotype influences baseline CD4+ T lymphocyte (CD4+) cell count and mortality of patients. The study was conducted from 2014 to 2019 in Guangxi, China, and included 2845 newly diagnosed HIV patients. We used a median regression model to compare CD4+ cell counts in patients newly diagnosed with different HIV-1 genotypes, and a Cox regression model to analyze the associations between HIV-1 genotypes and mortality before and after antiretroviral treatment (ART). In newly diagnosed HIV patients, the baseline CD4+ cell counts of patients with CRF01_AE were significantly lower than those of patients with CRF07_BC, CRF08_BC, and other genotypes. Compared with CRF01_AE, patients infected with CRF07_BC (hazard ratio, 0.55; 95% CI 0.36–0.85), CRF08_BC (hazard ratio, 0.67; 95% CI 0.52–0.85), or other genotypes (hazard ratio, 0.52; 95% CI 0.29–0.94) had significantly lower mortality rates before ART. There were no significant associations between different HIV-1 genotypes and mortality after ART. HIV-1 genotype significantly influences baseline CD4+ cell count and mortality before ART in newly diagnosed HIV patients. We find no significant difference in the outcome of death after ART in patients with different HIV-1 genotypes.

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Section: Discussionmentioning

confidence: 99%

Effects of HIV-1 genotype on baseline CD4+ cell count and mortality before and after antiretroviral therapy

Cao

Chen

et al. 2020

Sci Rep

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“…However, there is evidence that the viral quasispecies in plasma and the replication-competent HIV-1 variants in productively infected cells are closely related, if not the same viral compartments. Indeed, the kinetics of viral load changes and the emergence of drug resistance mutations in plasma/serum and productively infected cells are highly correlated (45)(46)(47). Moreover, an interesting aspect of our approach is that it allowed us to directly compare replication capacity in relation to sequence diversity.…”

Section: Discussionmentioning

confidence: 99%

Viral Replication Capacity as a Correlate of HLA B57/B5801-Associated Nonprogressive HIV-1 Infection

Navis

Schellens

Baarle

et al. 2007

The Journal of Immunology

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HLA B57 and the closely related HLA B5801 are over-represented among HIV-1 infected long-term nonprogressors (LTNPs). It has been suggested that this association between HLA B57/5801 and asymptomatic survival is a consequence of strong CTL responses against epitopes in the viral Gag protein. Moreover, CTL escape mutations in Gag would coincide with viral attenuation, resulting in low viral load despite evasion from immune control. In this study we compared HLA B57/5801 HIV-1 infected progressors and LTNPs for sequence variation in four dominant epitopes in Gag and their ability to generate CTL responses against these epitopes and the autologous escape variants. Prevalence and appearance of escape mutations in Gag epitopes and potential compensatory mutations were similar in HLA B57/5801 LTNPs and progressors. Both groups were also indistinguishable in the magnitude of CD8+ IFN-γ responses directed against the wild-type or autologous escape mutant Gag epitopes in IFN-γ ELISPOT analysis. Interestingly, HIV-1 variants from HLA B57/5801 LTNPs had much lower replication capacity than the viruses from HLA B57/5801 progressors, which did not correlate with specific mutations in Gag. In conclusion, the different clinical course of HLA B57/5801 LTNPs and progressors was not associated with differences in CTL escape mutations or CTL activity against epitopes in Gag but rather with differences in HIV-1 replication capacity.

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“…Moreover, phylogenetic analysis of env sequences shows that the viral quasispecies in plasma and isolated replication competent clonal HIV-1 variants from similar time points from the same individual are very closely related (Navis et al manuscript in preparation). Finally, it has been shown that the kinetics of viral load changes and the emergence of drug resistance mutations in plasma/serum and productively infected cells are highly correlated [40]–[42].…”

Section: Discussionmentioning

confidence: 99%

Molecular Evolution of Human Immunodeficiency Virus Type 1 upon Transmission between Human Leukocyte Antigen Disparate Donor-Recipient Pairs

et al. 2008

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BackgroundTo address evolution of HIV-1 after transmission, we studied sequence dynamics in and outside predicted epitopes of cytotoxic T lymphocytes (CTL) in subtype B HIV-1 variants that were isolated from 5 therapy-naive horizontal HLA-disparate donor-recipient pairs from the Amsterdam Cohort Studies on HIV-1 infection and AIDS.Methodology/Principal FindingsIn the first weeks after transmission, the majority of donor-derived mutations in and outside donor-HLA-restricted epitopes in Gag, Env, and Nef, were preserved in the recipient. Reversion to the HIV-1 subtype B consensus sequence of mutations in- and outside donor-HLA-restricted CTL epitopes, and new mutations away from the consensus B sequence mostly within recipient-HLA-restricted epitopes, contributed equally to the early sequence changes. In the subsequent period (1–2 years) after transmission, still only a low number of both reverting and forward mutations had occurred. During subsequent long-term follow-up, sequence dynamics were dominated by forward mutations, mostly (50–85%) in recipient-HLA-restricted CTL epitopes. At the end of long-term follow-up, on average 43% of the transmitted CTL escape mutations in donor-HLA-restricted epitopes had reverted to the subtype B consensus sequence.Conclusions/SignificanceThe relatively high proportion of long-term preserved mutations after transmission points to a lack of back selection even in the absence of CTL pressure, which may lead to an accumulating loss of critical CTL epitopes. Our data are supportive for a continuous adaptation of HIV-1 to host immune pressures which may have implications for vaccine design.

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Efficient inhibition of both syncytium-inducing and non-syncytium-inducing wild-type HIV-1 by lamivudine in vivo

Abstract: These data show that, in contrast to didanosine and zidovudine, the pressure exerted by 3TC is similar for SI and NSI M184 populations.

Cited by 7 publications

References 42 publications

Effects of HIV-1 genotype on baseline CD4+ cell count and mortality before and after antiretroviral therapy

Effects of HIV-1 genotype on baseline CD4+ cell count and mortality before and after antiretroviral therapy

Viral Replication Capacity as a Correlate of HLA B57/B5801-Associated Nonprogressive HIV-1 Infection

Molecular Evolution of Human Immunodeficiency Virus Type 1 upon Transmission between Human Leukocyte Antigen Disparate Donor-Recipient Pairs

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