Modern view on the features of the development and course of the antiviral immune response

Abstract

The review article summarizes recent literature data on immunopathogenetic features that influence the nature of the development and course of viral infections.
 According to the impact on a cell, cytopathic and non-cytopathic viruses are isolated. The course of viral infections is accompanied by cell death, immunopathology, immunosuppression, oncogenesis, and in later stages molecular mimicry and immune amnesia. The acute course of infections is controlled mainly by the mechanisms of innate immunity. The severity of the course of such infections is associated with the genetic variability of viruses and resistance to the antibodies' neutralizing effects. Viruses that are non-cytopathic in their natural mouse hosts can cause acute and chronic infections in humans. The activity of viral reproduction, the persistent infection may be associated with the peculiarities of the expression of gene profiles of the infected cell. The synthesis of endogenous interferons can also affect the nature of the infection development. Disturbances in signaling through Toll-like receptors may contribute to the persistence of infection. Some of the viral proteins block the presentation by the molecules of the main histocompatibility complex of I, II class of viral antigens, interfering with various stages of the presentation. This process is facilitated by a decrease in the transcription of genes of the main histocompatibility complex, blocking the secretion of immunogenic peptides by the proteasome or interfering with the subsequent assembly and transport of the peptide complex to the cell surface. A number of viral proteins stimulate the virus reproduction and inhibit apoptosis. It is believed that the B7-2 molecule is most important for triggering the immune response. Immunodominant epitopes of viral antigens, mutants of cytotoxic lymphocytes are key factors in the immunopathogenesis of persistent, latent infections. Changes in the viral genome of even a single amino acid allow them to avoid recognizing epitopes by an activated T-lymphocyte. Another mechanism for viruses to escape the immune system control is the death of activated T-cells.