Individuals with chronic infections like malaria and hepatitis are less likely to have the fullest immunity benefits from vaccines from unrelated illnesses, new studies have found.

The effect of bystander infections also extended beyond mice. The researchers generated signatures of transcribed genes of cytomegalovirus-specific T cells from people with chronic hepatitis C infection and healthy controls. The gene-expression profiles of these two groups showed a clear impact of bystander chronic infection on T cells, including a difference in expression of many key T-cell memory-related genes. The findings are published this week in Immunity.
"Co-infections can result in poor immunity for other invading microbes and also vaccines," says senior author E. John Wherry, PhD, director, Institute for Immunology and associate professor of Microbiology. "We now understand one of the main reasons: failure to develop immune memory capable of responding upon new infections."
Immune memory, the hallmark of protective immunity against intracellular pathogens, is what keeps humans from being reinfected by a microbe to which they have already been exposed. Some immune cells are long-lived and active against whatever they were originally triggered by.
"If a person in the developing world gets a vaccine, and they harbor unrelated infections, such as malaria, tuberculosis, hepatitis B or C, and other parasitic infections, will this person have effective immune memory to the vaccine?" asks Wherry. "Our study has major relevance for applying vaccines in the developing world where co-infections might radically alter the type and quality of immunity generated by vaccines."
Wherry cites vaccine campaigns for rotavirus and polio virus in the developing world in which people who were vaccinated had only 50 percent efficacy compared to 80 to 90 percent in the developed world for the same vaccine. Vaccine efficacy is the incidence of people who are vaccinated and get disease versus an unvaccinated control group.
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The team concluded that exposure to prolonged bystander inflammation impairs the transition of effector T cells to memory T cells. In other words, bystander chronic infections prevent the critical ability of the immune response to "stand down" and preserve responsive cells for future encounters with the same infection.
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Source-Eurekalert