Viruses such as HIV or hepatitis C virus (HCV) can destroy the immune system. So far, one way to develop vaccines against these chronic infections is to target memory B cells, a specific type of immune cell. In a new study, researchers from the University of Basel in Switzerland found that these cells need the help of other memory cells to effectively protect the body from chronic infections. This is an important discovery in vaccine design. The results of the study were recently published in PNAS, and the paper is entitled “Vaccine-elicited CD4 T cells prevent the deletion of antiviral B cells in chronic infection”.
A series of immune cells in the body can protect the body from pathogens. During virus infection, B cells produce antibodies that match and deactivate the virus. Some of these B cells die after infection or vaccination. However, some B cells remain in the body as memory cells to produce the correct antibodies more quickly in the event of a new infection with the same pathogen. One of the purposes of the vaccine is to trigger the production of these memory B cells.
However, viruses such as HIV or HCV inhibit the defense capabilities of memory B cells, hindering the development of an efficient vaccine. To overcome, a team led by Dr. Daniel Pinschewer of the Department of Biomedicine at the University of Basel studied the interaction between immune cells in chronic viral infections.
“One problem is that memory B cells enter a state of panic because of the persistence of pathogens and associated inflammation,” Pinschewer explained, “they abandoned the conventional route of proliferation and maturation and turned to the mode of antibody production, which soon died out.” They reported that there may now be a solution to the problem.
In their experiment, the authors studied infecting mice with a mouse virus called lymphocytic choroid plexus meningitis virus (LCMV), which causes chronic infection. They note that in order to respond continuously to the virus, memory B cells need the help of other immune cells like memory helper T cells, whose formation can also be triggered by appropriate vaccine strategies.
If the researchers induced mice to produce appropriate memory helper T cells before they were infected with LCMV, these memory helper T cells would prevent the panic response of memory B cells after infection. “Due to the existence of memory helper T cells, B cells are not depleted in the fight against the virus, which continue to proliferate and mature and maintain resistance to this virus infection,” said lead author Dr Kerstin Narr of the Department of Biomedicine at the University of Basel.
So far, the role of these memory helper T cells in vaccine against chronic viruses has not been fully studied, according to the authors. “Using these cells to promote a more lasting immune response by memorizing B cells is directly related to the strategy of developing new HIV and HCV vaccines.” Pinschewer said.