ArticleJournal of virology2002
Highly pathogenic simian immunodeficiency virus mne variants that emerge during the course of infection evolve enhanced infectivity and the ability to downregulate CD4 but not class I major histocompatibility complex antigens.
Article in Journal of virology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 18 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
18 citing papers in PubMed, 26 citations in OpenAlex.
- Vpx is critical for SIVmne infection of pigtail macaques.Retrovirology · 2012Article
- Vif substitution enables persistent infection of pig-tailed macaques by human immunodeficiency virus type 1.Journal of virology · 2011Article
- Relative replication capacity of phenotypic SIV variants during primary infections differs with route of inoculation.Retrovirology · 2010Article
- Counteraction of HLA-C-mediated immune control of HIV-1 by Nef.Journal of virology · 2010Article
- Dendritic cell-mediated HIV-1 infection of T cells demonstrates a direct relationship to plasma viral RNA levels.Journal of acquired immune deficiency syndromes (1999) · 2010Article
- HIV-1 Transmission, Replication Fitness and Disease Progression.Virology : research and treatment · 2008Article
- Article
- Phenotypic and genotypic comparisons of human T-cell leukemia virus type 1 reverse transcriptases from infected T-cell lines and patient samples.Journal of virology · 2007Article
- Contribution of Vpu, Env, and Nef to CD4 down-modulation and resistance of human immunodeficiency virus type 1-infected T cells to superinfection.Journal of virology · 2006Article
- Simian immunodeficiency virus variants that differ in pathogenicity differ in fitness under rapid cell turnover conditions.Journal of virology · 2005Article
- Primary sooty mangabey simian immunodeficiency virus and human immunodeficiency virus type 2 nef alleles modulate cell surface expression of various human receptors and enhance viral infectivity and replication.Journal of virology · 2005Article
- Human immunodeficiency virus type 1 inhibits DNA damage-triggered apoptosis by a Nef-independent mechanism.Journal of virology · 2005Article
- Analysis of pigtail macaque major histocompatibility complex class I molecules presenting immunodominant simian immunodeficiency virus epitopes.Journal of virology · 2005Article
- Comprehensive analysis of nef functions selected in simian immunodeficiency virus-infected macaques.Journal of virology · 2004Article
- Nef proteins from simian immunodeficiency virus-infected chimpanzees interact with p21-activated kinase 2 and modulate cell surface expression of various human receptors.Journal of virology · 2004Article
- Nef stimulates human immunodeficiency virus type 1 replication in primary T cells by enhancing virion-associated gp120 levels: coreceptor-dependent requirement for Nef in viral replication.Journal of virology · 2004Article
- Down-modulation of mature major histocompatibility complex class II and up-regulation of invariant chain cell surface expression are well-conserved functions of human and simian immunodeficiency virus nef alleles.Journal of virology · 2003Article
- nef gene is required for robust productive infection by simian immunodeficiency virus of T-cell-rich paracortex in lymph nodes.Journal of virology · 2003Article
Corrections and comments
- Erratum issued
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The replicative, cytopathic, and antigenic properties of simian immunodeficiency virus (SIV) variants influence its replication efficiency in vivo. To further define the viral properties and determinants that may be important for high-level replication in vivo and progression to AIDS, we compared a minimally pathogenic SIVmne molecular clone with two highly pathogenic variants cloned from late stages of infection. Both variants had evolved greater infectivity than the parental clone due to mutations in nef. Interestingly, a pol determinant in one of the highly pathogenic variants also contributed to its increased infectivity. Furthermore, because replication in vivo may also be influenced by the ability of a virus to evade the cellular immune response of the host, we examined whether the variants were more capable of downregulating surface expression of class I major histocompatibility complex (MHC). Decreased MHC class I expression was not observed in cells infected with any of the viruses. Furthermore, the Nef proteins of the highly pathogenic variants only slightly reduced surface MHC class I expression in transfected cells, although they efficiently downregulated CD4. Together, these data demonstrate that mutations which can enhance viral infectivity, as well as CD4 downregulation, may be important for efficient replication of SIV in the host. However, Nef-mediated reduction of MHC class I expression does not appear to be critical for the increased in vivo replicative ability of highly pathogenic late variants.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.