Developing an effective anti tuberculosis (TB) vaccine is a top priority for global control of
TB. Since BCG has limited protection against Mycobacterium tuberculosis (MTB) infection, efforts
are being made to improve its protective efficacy further. Prime-boost is a strategy whereby an
individual is primed with BCG followed by boosting with a heterologous anti TB vaccine/antigen. In
several instances, boosting involves up-modulation of CD4+ Th1 mediated cellular immunity by
stimulation with the corresponding antigen(s) as well as by down modulating the immunosuppressive
regulatory T cells. In a recent trial with such a booster candidate vaccine (MVA85A) against TB,
despite enhancing the IFN-γ+CD4+Th1 mediated immunity, no significant improvement in protective efficacy against TB
was observed in the vaccinated group. A possible cause for under performance of this vaccine could be the lack of killing
of MTB by invaded antigen presenting cells (APCs) such as macrophages and dendritic cells (either due to MTB itself or
due to polymorphisms in interferon-γ receptors). Consequently, MTB would survive and multiply inside APCs and would
lead to the development of TB reflecting the non-efficacy of the vaccine. In this communication, a concise description
about the probable reasons for poor performance of MVA85A in providing protection against TB has been put forth.
Keywords: Tuberculosis, vaccine, Tregs, MVA85A.
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