Official websites use. Share sensitive information only on official, secure websites. Within the first weeks of human immunodeficiency virus HIV infection, virus replication reaches systemic circulation. Despite the critical, causal role of virus replication in determining transmissibility and kinetics of disease progression, there is limited understanding of the conditions required to transform a small localized transmitted founder population into a large and heterogeneous systemic infection.
Cynomolgus and rhesus macaques were infected with simian immunodeficiency virus SIV and followed longitudinally. Flow cytometry was used to track peripheral blood lymphocyte populations. In vitro assays were performed by exposing freshly isolated peripheral blood mononuclear cells to bacterial lysate prepared from major translocators. Prior to the peak of viremia, we observed a transient high-level influx of microbial genomic DNA into peripheral blood. Altogether, our data identify the influx of microbial products into blood during hyperacute SIV infection as a candidate modifier of early interactions between the antiviral host response and nascent HIV infection.
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High dietary fats were reported to induce intestinal dysbiosis, drive gut inflammation and breakdown the intestinal epithelial barrier, granting intestinal flora access to the bloodstream. The non-progressive African green monkey AGM model of SIV is an ideal system to assess the role of fat diet on disease progression, because they do not develop SIV-related intestinal dysfunction.
Furthermore, these changes did not result in significant increases in the levels of viral replication in the AGMs receiving a fat diet.
Administration of fat-rich diet resulted in alterations of markers of pathogenicity in the non-progressive SIV infection of AGMs. Although not major, these changes were significant, suggesting that a diet very rich in fats may negatively impact HIV pathogenesis, especially if combined with other behavioural risk factors reported to impact gut integrity or systemic inflammation, such as alcohol consumption, drug usage and smoking.
