Mechanism by Which HIV Turns Food Poisoning into Lethal Infection Unveiled

Research at UC Davis co-authored by an Indian origin scientist has discovered a mechanism by which HIV turns food poisoning into fatal infection using an animal study.

Research at University of California - Davis (UC Davis) co-authored by an Indian origin scientist has discovered a mechanism by which HIV turns food poisoning into fatal infection using an animal study.

Nearly half of all HIV-positive African adults who become infected with salmonella bacteremia die from what otherwise would be a seven-day bout of diarrhea.

ow, a team of researchers along with Satya Dandekar has found that a defect in the immune response is what is responsible for Salmonella to cause such a deadly infection.

"We have found the defect in the immune response that allows Salmonella to cross the mucosal barrier of the gut, enter the bloodstream and infect other organs," Nature quoted Andreas Bäumler, a UC Davis professor of medical microbiology and immunology and co-author of the study, as saying.

Viral infection of the intestine results in the depletion of a type of white blood cell, called Th-17, in the gut mucosa.

This white blood cell in turn produces IL-17, a cytokine or chemical messenger that plays a crucial role in the immune system's response. It brings other immune system cells to the site of infection.

An interruption of this response in the gut could also be how HIV evades the powerful drugs used to treat AIDS.

"We think the real battle between an individual's immune system and HIV is happening in the gut mucosa where there is massive destruction of immune cells," said Satya Dandekar, professor and chair of the department of medical microbiology and immunology.

In HIV-infected patients, there is a gradual loss of T helper cells CD4+ T that organize the immune system's attack on viruses. In the gut mucosa however, this decline is very rapid.

The researchers found that animals infected with simian immunodeficiency virus (SIV), an established model for HIV infection, had either a significantly lower response or did not produce measurable amounts of the Th17 cells in large amounts.

This muted response, the boffins stated, is used by Salmonella to travel from the gut to the peripheral blood.

Using mice, they confirmed that the deficiency of the IL-17 receptor, an arm of the mucosal immune response, causes defects in the mucosal barrier of the gut, helping Salmonella travel.

The results of the study were published online by Nature Medicine March 23.

Source-ANI
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