HIV-1 viraemia and influenza

Dd, Ho

doi:10.1016/0140-6736(92)91321-x

Cited by 108 publications

(52 citation statements)

References 1 publication

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…During the generation of immune responses, tissue DC (that are either infected with HIV or that capture virus en route to lymph nodes) may activate and infect TC concomitantly, and thus contribute to Ag-specific depletion of TC. Consistent with this theory, increases in viral replication have been documented after vaccination and acute illnesses in HIVinfected individuals (45)(46)(47)(48)(49). Thus, blocking DC-mediated infection of TC may be an important strategy for the treatment of HIV disease.…”

Section: Discussionmentioning

confidence: 58%

Productive infection of dendritic cells by HIV-1 and their ability to capture virus are mediated through separate pathways.

Blauvelt¹,

Asada²,

Saville³

et al. 1997

J. Clin. Invest.

183

165

View full text Add to dashboard Cite

There is substantial evidence that dendritic cells (DC) residing within epithelial surfaces (e.g., Langerhans cells) are the initial cells infected with HIV after mucosal exposure to virus. To study DC-HIV interactions in detail, we propagated Langerhans cell-like DC from cord blood CD34 ϩ cells and from adult blood plastic-adherent PBMC in the presence of cytokines (GM-CSF, IL-4, and/or TNF-␣ ). DC pulsed overnight with HIV BaL or HIV IIIB were infected productively with both viral subtypes (as assessed by PCR, supernatant p24 protein levels, electron microscopy, and antibody staining). Productive infection could be blocked by anti-CD4 mAbs, RANTES (regulated upon activation, normal T cell expressed and secreted) (for HIV BaL ), stromal cell-derived factor-1 (for HIV IIIB ), or azidothymidine added during the HIV pulse, as well as by blocking DC proliferation. However, pulsing DC with HIV under these blocking conditions had no effect on the ability of DC to capture virus and transmit infection to cocultured antigen-stimulated CD4 ϩ T cells. Thus, we show by several criteria that ( a ) productive infection of DC and ( b ) the ability of DC to capture virus are mediated through separate pathways. We suggest that strategies designed to block mucosal transmission of HIV should consider interfering with both virus infection and virus capture by DC. (

show abstract

Section: Discussionmentioning

confidence: 58%

Productive infection of dendritic cells by HIV-1 and their ability to capture virus are mediated through separate pathways.

Blauvelt¹,

Asada²,

Saville³

et al. 1997

J. Clin. Invest.

183

165

View full text Add to dashboard Cite

show abstract

“…Viremia, a simple and widely used marker, may arise from viral cycling between different tissues and perhaps subtly different cell subsets, as well as reflecting bursts resulting from antigenic stimulation (47)(48)(49). Hence, in addition to entry and transactivation elements, LTR genetic polymorphisms can contribute substantially to the differential replication and dissemination of HIV/SIV in vivo.…”

Section: Discussionmentioning

confidence: 99%

HIV-1 clade promoters strongly influence spatial and temporal dynamics of viral replication in vivo

Centlivre

Sommer²,

Michel³

et al. 2005

J. Clin. Invest.

View full text Add to dashboard Cite

Although the primary determinant of cell tropism is the interaction of viral envelope or capsid proteins with cellular receptors, other viral elements can strongly modulate viral replication. While the HIV-1 promoter is polymorphic for a variety of transcription factor binding sites, the impact of these polymorphisms on viral replication in vivo is not known. To address this issue, we engineered isogenic SIVmac239 chimeras harboring the core promoter/enhancer from HIV-1 clades B, C, and E. Here it is shown that the clade C and E core promoters/enhancers bear a noncanonical activator protein-1 (AP-1) binding site, absent from the corresponding clade B region. Relative ex vivo replication of chimeras was strongly dependent on the tissue culture system used. Notably, in thymic histocultures, replication of the clade C chimera was favored by IL-7 enrichment, which suggests that the clade C polymorphism in the AP-1 and NF-κB binding sites is involved. Simultaneous infection of rhesus macaques with the 3 chimeras revealed a strong predominance of the clade C chimera during primary infection. Thereafter, the B chimera dominated in all tissues. These data show that the clade C promoter is particularly adapted to sustain viral replication in primary viremia and that cladespecific promoter polymorphisms constitute a major determinant for viral replication.

show abstract

“…[9,11], but so far vaccination has not been regarded as unsafe for HIV + individuals. The viraemia following immunization occurs rapidly and declines equally fast in accordance with recent knowledge about the rapid immune response to influenza vaccination that takes place in lymphatic tissues [20].…”

Section: Discussionmentioning

confidence: 99%

“…Some reports indicated an increase in blood levels of HIV in the vaccine recipients, whereas others where unable to confirm this [9,10]. Vaccination with T cell-dependent immunogens leads to T cell activation and proliferation, which in turn could enhance HIV replication and thereby result in measurable increases in blood levels of HIV.…”

Section: Introductionmentioning

confidence: 99%

Dynamics of HIV-1 replication following influenza vaccination of HIV+ individuals

Røsok¹,

Voltersvik²,

Bjerknes³

et al. 1996

Clinical and Experimental Immunology

View full text Add to dashboard Cite

Levels of HIV‐1 have been reported to increase in peripheral blood after influenza vaccination of HIV+ individuals. In this study we have evaluated the dynamics of these changes. Ten HIV‐1+ individuals classified in revised CDC clinical categories B and C as well as five seronegative healthy controls were vaccinated with the recommended influenza strains. HIV viral RNA and proviral DNA were sequentially quantified in serum and blood lymphocytes, respectively. Nine of the 10 HIV+ individuals had an increase in the frequency of infected CD4 cells 2 weeks after influenza vaccination. Individuals with low viral load had a rapid increase in viraemia and a small increase in frequency of infected cells in peripheral blood. In contrast, individuals with high viral load had a small drop in viraemia followed by a significant rise in the rate of infected cells. The observed changes may resemble those taking place during intercurrent infections in HIV+ individuals. The effects of the relative increases in infectious virus after the transient viraemic phase should be further investigated to evaluate potential risks of vaccination.

show abstract

HIV-1 viraemia and influenza

Cited by 108 publications

References 1 publication

Productive infection of dendritic cells by HIV-1 and their ability to capture virus are mediated through separate pathways.

Productive infection of dendritic cells by HIV-1 and their ability to capture virus are mediated through separate pathways.

HIV-1 clade promoters strongly influence spatial and temporal dynamics of viral replication in vivo

Dynamics of HIV-1 replication following influenza vaccination of HIV+ individuals

Contact Info

Product

Resources

About