by The researchers suspect that the way cells use nutrients in the presence of a virus may determine the outcome and severity of the disease.
The immune system has long been touted as the body’s primary defense against invading viruses, with the understanding that a strong immune response quickly clears an infection, while a weak one allows it to linger, leading to prolonged illness or disease. even to death.
Now, researchers are looking at an entirely different system, the body’s ability to use nutrients at the cellular level, to predict disease response and severity.
Tulane University immunologist Clovis Palmer studies the metabolic changes that result from viral infections. In a review of the literature on Nature MetabolismPalmer reviewed a body of evidence that looked at the metabolic changes that occur in cells when viral invaders, such as HIV, hepatitis B, or SARS-CoV-2, pose a threat.
Palmer concludes that the way in which cells, even non-immune cells, use nutrients in the presence of a viral pathogen can determine the outcome and severity of the disease early in the infection, or even long after the infection has passed. pathogen leaves the body.
Certain molecules on the surface of a cell determine how nutrients are used. These allow nutrients like glucose and fat to facilitate energy production or, if necessary, mount an offensive against invading pathogens. Under these conditions, the nutrients strengthen and reinforce the cell. But viral pathogens can also hijack these surface molecules to enter the cell and then use the nutrients to replicate.
“Whether the nutrients are used to strengthen and defend the cell or whether they are sequestered by the virus depends on host conditions, such as advanced age, nutritional status, and obesity,” says Palmer. “We saw that all of these were significant risk factors for worse COVID outcomes, but we didn’t really know what was driving it.”
Understanding how cells use nutrients in the presence of viral pathogens in the early stages of infection is key to developing treatments that can strengthen the cell, not the virus. While most antiviral drugs target the virus, Palmer seeks to prevent or lessen disease by keeping nutrients on the cell’s side.
Palmer is working with Jay Rappaport, director of the Tulane National Primate Research Center and professor of microbiology and immunology at Tulane University School of Medicine, on reconfiguring the metabolic response in nonhuman primate models of COVID and HIV to prevent and treat long-term symptoms.
“We know that when metabolism is affected, susceptibility to infection increases,” says Rappaport. “Modulating the metabolic response has broad implications for all infectious diseases, from optimizing immunity to mitigating the effects of aging, autoimmunity, and other drivers of disease.”
Source: Tulane University
