Aktywność cytotoksyczna efektorowych limfocytów T w ostrych i

POST. MIKROBIOL.,
1999, 38, 4, 355
AKTYWNOŚC CYTOTOKSYCZNA
EFEKTOROWYCH LIMFOCYTÓW T
W OSTRYCH I PERSYSTENTNYCH/LATENTNYCH
ZAKAZENIACH HERPESWIRUSOWYCH I HIV:
TESTAMENT ZAKAŻONEJ KOMÓRKI
Marek G. Niemiałtowski
Felix, qui pótuit rerum cognóscere cáusas
Szczęśliwy, kto mógł poznać praprzyczyny spraw
Vergilius
1. Wstęp. 2. Co to jest zakażenie ostre, persystentne i latentne? 3. Rola antygenu wirusowego w
rozwoju pamięci immunologicznej. 4. Cytotoksyczne limfocyty T w zakażeniach ostrych oraz
persystentnych i latentnych na przykładzie herpeswirusów i retrowirusów (HIV). 4.1. Herpesviridae.
4.1.1. Herpeswirusy α. 4.1.2. Herpeswirusy β. 4.1.3. Herpeswirusy γ. 4.2. Rodzina Retroviridae.
4.2.1. Wirus nabytego braku odporności ludzi (HIV). 5. Porównanie aktywności wirusowo-swoistych
CTL w zakażeniu herpeswirusami i HIV. 6. Modulacja apoptozy przez herpeswirusy i HIV.
7. Podsumowanie
Cytotoxic activity of effector T Iymphocytes in acute and persistent/latent viral
infections: a testament of an infected cell
Abstract:
The establishment of persistent/latent viral infections is affected by many
factors associated with the biological activity of viruses and the infected host, and the
environment in which both the host and the infecting agent reside. Development of persistent
and latent viral infections in humans and animals apparently influences the evolution of the
immune system as a whole, particularly its individual components. Maintaining the
equilibrium between the aggressor (virus) and the victim (host) is paramount to the imposed
coexistence whose consequence is not only preservation of the individual elements of this
refined biological system, but also conservation of the species with intact features. Viruses
have developed subtle strategies that allow persistence in the infected host, including escape
from immune surveillance through (i) latency, (ii) interaction with various components of the
immune system (iii) virus induced modulation of immune cell surface structures, which
binders or disables recognition of foreign antigens by immunocompetent cells e.g., virusspecific CTL, (iv) molecular mimicry, (v) modulation of MHC class I and/or class II on the
infected cell surface, (vi) the possibility of viruses to encode immunosuppressive cytokines,
and (vii) modulation of apoptosis. Therefore, each infected cell, early during infection or late
in persistent or latent infection, writes its own biotestament and dedicates its life span
defending the host against development of disease and ultimate death. Precise understanding
of the mechanisms involved in the immunobiology of viral infections will certainly enable
development of more effective prophylactic methods and antiviral agents.
1. Introduction. 2. What is acute, persistent and latent infection? 3. The role of viral antigen in
development of immunological memory. 4. Cytotoxic T lymphocytes in acute and persistent/latent
infections on example of herpesviruses and retroviruses (HIV). 4.1. Herpesviridae.
4.1.1. Herpesviruses α. 4.1.2. Herpesviruses β. 4.1.3. Herpesviruses γ. 4.2. Retroviridae 4.2.1. Human
immunodeficiency virus (HIV). 5. Comparison of the activity of virus-specific CTL in herpesvirus
and HIV infections. 6. Modulation of apoptosis by herpesviruses and HIV. 7. Summary