Page 897 - Veterinary Immunology, 10th Edition
P. 897

herpesvirus infection. Some time later, however, especially when
  VetBooks.ir  the individual is stressed, the herpesvirus may reappear and may

               even cause disease. During the latent period, when it is present in
               the host but cannot be reisolated, the virus nucleic acid persists in

               host cells, but its transcription is blocked, and viral proteins are not
               made. The persistent virus may periodically boost the immune
               response of the infected animal and in this way generate long-
               lasting immunity to superinfection. The immune responses in these

               cases, although unable to eliminate viruses, may prevent the
               development of clinical disease and therefore serve a protective
               role. Immunosuppression or stress may permit disease to occur in
               persistently infected animals. The association between stress and

               the development of some virus diseases is well recognized. It is
               likely that the increased steroid production in stressful situations
               may be sufficiently immunosuppressive to permit activation of
               latent viruses or infection by exogenous ones.

                  Sometimes viruses may interact with bacteria to overcome the
               immune system. For example, Mannheimia hemolytica and bovine
               herpesvirus (BHV-1), acting together, cause severe respiratory
               disease in cattle. BHV-1 infection increases expression of the β -
                                                                                                  2
               integrin LFA-1 on lung neutrophils. The leukotoxin of M. hemolytica
               binds to this integrin and then kills the neutrophils, permitting

               growth of the invading bacteria.


               Inhibition of Apoptosis


               Apoptosis may be considered a protective response since viruses
               also die when a cell dies. This is especially significant if a cell dies

               before viruses are released. It is therefore to a virus's advantage to
               delay apoptosis until progeny viruses can be released. Thus cowpox
               and some herpesviruses (including equine herpesvirus-2) encode
               apoptosis inhibitors in their genomes. Viruses may also benefit by

               killing cells of the immune system. Rapidly dividing lymphocytes
               are susceptible to death signals. For example, lymphoid cell
               apoptosis is a feature of canine distemper, a disease characterized
               by severe immunosuppression (Chapter 40).










                                                         897
   892   893   894   895   896   897   898   899   900   901   902