When infectious virus enters the body by the so called portal of entry it may:
1. Replicate in susceptible cells
2. Behave as a foreign antigen (and/or antigen mix).
Which cells are upmost important to restrict productive virus replication and/or dissemination, when they contemporarily initiate the immune response?
Which is the molecular mechanism of the restrictive behaviour of mononuclear phagocytes (macrophes)?
Step by step:Nonspecific immune reaction: Compliment and B - cell (extract IgM). These attract macrophages, and Th1/Th2, and T(CD8+).
Major restriction appears to bemanaged by Ag-presenting T cells to T-killers.
Nonspecific behavior of macrophages is expressed in two mechanisms: agent absorption, and extraction of vasoactive elements and interleukins. They increase the temperature of the infection focus and attract the migration of T-killers and T-helpers to the focus of infection.
This is all correct. But what I had in mind is the dual behaviour of phagocytes. In cases of efficiently virulent virus strains the mononuclear white blood cells would replicate and disseminate the virus (examples: measles, yellow fever, dengue and several others).
Dear Julius, there are two general specific mechanisms restricting dissemination of viruses. First one is CTL which kill infected cells thus eliminating viral replication. Second mechanism is neutralization of viral particles by antibodies produced by B cells. So, in classical works written by Rolf Zinkernagel and co-authors we frequently see investigations of both mechanisms together. As a rule, phagocytes are terminally differentiated not dividing cells thus providing poor environment for viral replication. Against, lymphocytes are frequently used by different viruses for replication. Restricting mechanism for this we can see as deletion of subpopulations of T cells responding on viral superantigens (good example is MMTV causing depletion of T cells with specific Vbetas). As the newest entity, I should notice CD103-positive intraepithelial resident memory T cells capable to very fast local activation in barrier tissues upon viral penetration. They could provide early protection from viral replication in any host cells.
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