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Examples include most viruses that infect humans, such as those that
cause routine respiratory infections (e.g. cold viruses, influenza viruses) and
gastrointestinal infections (e.g. Rotaviruses, Noroviruses).
I. Viral Latency:
Viral latency is the ability of a pathogenic virus to lie dormant within a
cell, usually denoted as the lysogenic part of the viral life cycle. A latent viral
infection is known to be a type of persistent viral infection, and is distinguis-
hed from a chronic viral infection.
Since the viral genome is not fully eradicated from the body of the host,
a latent virus can be reactivated and begin producing large amounts of viral
progeny without the host being infected by new outside virus, (denoted as
the lytic part of the viral life cycle), and stays within the host indefinitely.
Latency in Bacteriophages:
Advantages of episomal latency include the fact that the virus may not
need to enter the nucleus, and hence may avoid ND10 domains from
activating interferon via that pathway.
B. Proviral latency:
Proviral latency occurs when the virus genome integrates into the host
genome, effectively becomes a provirus. This requires that the viral gene get
into the nucleus and insert itself into the host genome.
Disadvantages include the need to enter the nucleus (and the need
for packaging proteins that will allow for that) and increased difficulty in
maintaining the latency.
For a virus to survive, it must elude the ever vigilant immune sentinels
of its host. A latent virus can escape immune detection if it resides in non-
dividing cells and doesn’t produce any proteins. No viral proteins means no
red flags for immune cells. If the virus targets one of the many cell types that
rarely divide, it’s relatively safe while latent.
Lab studies show that the amino acid element limits EBNA-1’s
interaction with T cells by inhibiting synthesis and, to a lesser degree,
degradation of the protein. This results in impairing antigen processing and
MHC class I-restricted antigen presentation, thereby inhibiting the CD8-
restricted cytotoxic T cell response against virus-infected cells.
How this evasive action works or helps the virus in a living organism is
not entirely clear. But if T cells aren’t presented with bits of viral protein, they
have no way of knowing the virus is present.
While viral latency exhibits no active viral shedding nor causes any
pathologies or symptoms, the virus is still able to reactivate via external
activators (i.e. sunlight, stress) to cause an acute infection. In case of
Herpes simplex virus, which generally infects an individual for life, a serotype
of the virus reactivates occasionally to cause cold sores.
The sores are quickly resolved by the immune system, however may
be a minor annoyance from time to time.
B | Upon reactivation, viral lytic gene expression is initiated, and newly formed
capsids are transported to the axonal termini. Infectious virus is released from
the axon and infects epithelial cells, resulting in recurrent infection and virus
shedding.
Viral Targets - EBV only infects a small number of cell types that
express the receptor for complement C3d component (CR2 or CD21). These
are certain epithelial cells (oro- and naso-pharynx) and B lymphocytes.
This explains the cellular tropism of the virus.
Life cycle - Virus infection involves two types of cells: (1) B cells,
where infection is predominantly latent and has the potential to induce
growth-transformation of infected cells; and (2) Epithelial cells, where
infection is predominantly replicative. EBV latent infection of B-lymphocytes
is necessary for virus persistence, subsequent replication in epithelial cells,
and release of infectious virus into saliva.