[Prevention and therapy of herpesvirus infections].
The group of the human-pathogenic herpesviruses comprises five subgroups: Herpes simplex virus type 1 (HSV-1), Herpes simplex virus type 2 (HSV-2), varicella zoster virus (VZV), cytomegalovirus (CMV), and Epstein-Barr virus (EBV). Primary infection with these ubiquitous herpesviruses usually occurs in childhood or during adolescence and frequently remains inapparent. However, it can also give rise to a variety of clinical pictures. Important clinical manifestations of herpesvirus infections are mucocutaneous lesions (HSV-1, HSV-2, VZV) self-limited, lymphoproliferative diseases (CMV, EBV) and congenital malformations (CMV). Primary infection with herpesviruses leads to a persistent infection of the host. This clinically silent condition of latency can be interrupted and may cause pathological symptoms to recur by reactivation of latent herpesviruses. A classical example of the clinical manifestation of herpesvirus reactivation is herpes zoster following an overcome varicella disease. The mechanism of herpesvirus reactivation has not yet been fully clarified. Reactivation of herpesviruses might be attributable to a weakening of the cellular immunodefence. For the control of viral infections mainly two cellular effector systems are responsible: unspecific, cytotoxic, natural killer (NK) cells and specific cytotoxic thymus-dependent (T) lymphocytes. The functional impairment of these cytotoxic active cells my cause herpesvirus reactivation in immunodeficient or immunosuppressed persons. Interference with the immunological control function may also contribute to the genesis of herpesvirus-associated tumours. Such an association between herpesviruses and human tumours is assumed to exist especially in the case of EBV. The frequently life-endangering severity of local or disseminated herpesvirus infections calls for suitable measures ensuring efficient prophylaxis and therapy. However, the possibilities of a specific immunoprophylaxis (vaccine, special immunoglobulins) against herpesvirus infections are still rather limited. The development of antiviral substances has greatly benefited from the introduction of new agents (Acyclovir) and the production of sufficient quantities of interferon (IFN) preparations during the last few years. Impressive results were obtained with the nucleoside-related substance Acyclovir in the prevention and therapy of primary or reactivated HSV-1 or HSV-2 infections. The use of Acyclovir as prophylactic agent produced the effect that recipients of bone-marrow transplants were no longer afflicted by HSV-1 infections.(ABSTRACT TRUNCATED AT 400 WORDS)
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D000212:Acyclovir / Q000627:therapeutic use; D000998:Antiviral Agents / Q000627:therapeutic use; D002051:Burkitt Lymphoma / Q000517:prevention & control; D002644:Chickenpox / Q000517:prevention & control; D003587:Cytomegalovirus / Q000472:pathogenicity; D003586:Cytomegalovirus Infections / Q000517:prevention & control; D005260:Female; D006558:Herpes Genitalis / Q000517:prevention & control; D006561:Herpes Simplex / Q000517:prevention & control; D006562:Herpes Zoster / Q000517:prevention & control; D006564:Herpesviridae / Q000276:immunology / Q000472:pathogenicity; D006566:Herpesviridae Infections / Q000188:drug therapy / Q000276:immunology / Q000517:prevention & control*; D014645:Herpesvirus 3, Human / Q000472:pathogenicity; D004854:Herpesvirus 4, Human / Q000472:pathogenicity; D006801:Humans; D007111:Immunity, Cellular; D007116:Immunization, Passive; D007244:Infectious Mononucleosis / Q000517:prevention & control; D008297:Male; D009303:Nasopharyngeal Neoplasms / Q000517:prevention & control; D018139:Simplexvirus / Q000472:pathogenicity; D012900:Smallpox Vaccine; D013601:T-Lymphocytes / Q000276:immunology; D014740:Vidarabine / Q000627:therapeutic use
D000998:Antiviral Agents; D012900:Smallpox Vaccine; D014740:Vidarabine; D000212:Acyclovir
Prophylaxe und Therapie von Herpesinfektionen.