Question

_What mechanisms do retroviruses use to limit reinfection of infected cells, and why they prevent reinfection?

_How HIV regulates timing of protein expression(some early, and some late)?

Answer 1

The early, nonspecific responses (nonspecific inhibition, natural killer cell activity, and interferon) limit virus multiplication during the acute phase of virus infections. The later specific immune (humoral and cell-mediated) responses function to help eliminate virus at the end of the acute phase, and subsequently to maintain specific resistance to reinfection.Immune-mediated disease may develop in certain virus infections in which viral antigens and uncontrolled immune hypersensitivity to them persist for a long period. Immune-mediated disease can be mediated by both humoral and cell-mediated immune functions. Immune-complex syndrome can be mediated by virus/virus antigen antibody complexes. T cells (cytotoxic and helper) can also mediate immunopathologic injuries via a number of mechanisms. Immunopathology can result from tissue/organ damage via cytotoxic T cells, inflammation induced via cytokines, antibody plus complement, antibody-antigen complexes and/or ADCC.

HIV regulates timing via diffrent kinds of regulatory proteins

These proteins are divided into three classes:

1. The major structural proteins, Gag, Pol, and Env

2. The regulatory proteins, Tat and Rev

3. The accessory proteins, Vpu, Vpr, Vif, and Nef

4. e.g. explanation of all genes iss quite lengthy so i used some of Gag -

   The gag gene gives rise to the 55-kilodalton (kD) Gag precursor protein, also called p55, which is expressed from the unspliced viral mRNA. During translation, the N terminus of p55 is myristoylated,(3) triggering its association with the cytoplasmic aspect of cell membranes. The membrane-associated Gag polyprotein recruits two copies of the viral genomic RNA along with other viral and cellular proteins that triggers the budding of the viral particle from the surface of an infected cell. After budding, p55 is cleaved by the virally encoded protease(4) (a product of the pol gene) during the process of viral maturation into four smaller proteins designated MA

   The MA polypeptide is derived from the N-terminal, myristoylated end of p55. Most MA molecules remain attached to the inner surface of the virion lipid bilayer, stabilizing the particle. A subset of MA is recruited inside the deeper layers of the virion where it becomes part of the complex which escorts the viral DNA to the nucleus.These MA molecules facilitate the nuclear transport of the viral genome because a karyophilic signal on MA is recognized by the cellular nuclear import machinery. This phenomenon allows HIV to infect nondividing cells, an unusual property for a retrovirus.