Virus latency

Source: Wikipedia, the free encyclopedia.
"Viral reservoir" redirects here. For a population of organisms in which a pathogen naturally lives and reproduces, see Natural reservoir.

Virus latency (or viral latency) is the ability of a

lytic part of the viral life cycle) without the host becoming reinfected by new outside virus, and stays within the host indefinitely.[2]

Virus latency is not to be confused with

clinical latency during the incubation period
when a virus is not dormant.

Mechanisms

Episomal latency

Episomal latency refers to the use of genetic

ribozymes
or host foreign gene degradation than proviral latency (see below).

Herpesviridae

One example is the

neurons and leave linear genetic material floating in the cytoplasm.[3]

Epstein-Barr virus

The

B-cells in the case of Epstein–Barr virus.[3][4] Epstein–Barr virus lytic reactivation (which can be due to chemotherapy or radiation) can result in genome instability and cancer.[5]

Herpes simplex virus

In the case of herpes simplex (HSV), the virus has been shown to fuse with

ganglia[6] or neurons, and HSV reactivates upon even minor chromatin loosening with stress,[7] although the chromatin compacts (becomes latent) upon oxygen and nutrient deprivation.[8]

Cytomegalovirus

Cytomegalovirus (CMV) establishes latency in myeloid progenitor cells, and is reactivated by inflammation.[9] Immunosuppression and critical illness (sepsis in particular) often results in CMV reactivation.[10] CMV reactivation is commonly seen in patients with severe colitis.[11]

Advantages and disadvantages

Advantages of episomal latency include the fact that the virus may not need to enter the

nuclear domain 10 (ND10) from activating interferon
via that pathway.

Disadvantages include more exposure to cellular defenses, leading to possible degradation of viral gene via cellular

enzymes.[12]

Reactivation

Reactivation may be due to stress,

UV light, etc.[13]

Proviral latency

A provirus is a virus genome that is integrated into the DNA of a host cell.

Advantages and disadvantages

Advantages include automatic host cell division results in replication of the virus's genes, and the fact that it is nearly impossible to remove an integrated provirus from an infected cell without killing the cell.[14]

A disadvantage of this method is the need to enter the nucleus (and the need for packaging proteins that will allow for that). However, viruses that integrate into the host cell's genome can stay there as long as the cell lives.

HIV

Further information: HIV latency

One of the best-studied viruses that does this is

antiretroviral drugs. Several classes of latency reversing agents (LRAs) are under development for possible use in shock-and-kill strategies in which the latently infected cellular reservoirs would be reactivated (the shock) so that anti-viral treatment could take effect (the kill).[15]

Maintaining latency

Both proviral and episomal latency may require maintenance for continued infection and fidelity of viral genes. Latency is generally maintained by viral genes expressed primarily during latency. Expression of these latency-associated genes may function to keep the viral genome from being digested by cellular

RNA transcripts such as non-coding RNAs and proteins) may also inhibit apoptosis or induce cell growth and division to allow more copies of the infected cell to be produced.[16]

An example of such a gene product is the

major histocompatibility complex (MHC) and inhibiting the apoptotic pathway.[17]

A certain type of latency could be ascribed to the endogenous retroviruses. These viruses have incorporated into the human genome in the distant past, and are now transmitted through reproduction. Generally these types of viruses have become highly evolved, and have lost the expression of many gene products.[18] Some of the proteins expressed by these viruses have co-evolved with host cells to play important roles in normal processes.[19]

Ramifications

While viral latency exhibits no active

herpes zoster
.

More serious ramifications of a latent infection could be the possibility of transforming the cell, and forcing the cell into

Necker Hospital in Paris, where twenty young boys received treatment for a genetic disorder, after which five developed leukemia-like syndromes.[20]

Human papilloma virus

This is also seen with infections of the

persistent infection may lead to cervical cancer as a result of cellular transformation.[21][22][23]

HIV

In the field of HIV research, proviral latency in specific long-lived cell types is the basis for the concept of one or more viral reservoirs, referring to locations (cell types or tissues) characterized by persistence of latent virus. Specifically, the presence of replication-competent HIV in resting CD4-positive T cells allows this virus to persist for years without evolving despite prolonged exposure to antiretroviral drugs.[24] This latent reservoir of HIV may explain the inability of antiretroviral treatment to cure HIV infection.[24][25][26][27]

See also

References

  1. ^ Villarreal, Luis P. (2005). Viruses and the Evolution of Life. Washington, ASM Press.
  2. ^ N.J. Dimmock et al. "Introduction to Modern Virology, 6th edition." Blackwell Publishing, 2007.
  3. ^
    PMID 16909907
    .
  4. PMID 17709530
    .
  5. PMID 27877083
    .
  6. PMID 28644417
    .
  7. ^ "Discovery shows how herpes simplex virus reactivates in neurons to trigger disease". 2015-12-21.
  8. ^ "Starve a Cell, Compact Its DNA - GEN". GEN. 2015-11-10.
  9. PMID 26572645
    .
  10. PMID 17922387
    .
  11. PMID 25684400
    .
  12. PMID 12573050
    .
  13. PMID 21348106
    – via PubMed.
  14. ^ Marcello A. "Latency: the hidden HIV-1 challenge." Retrovirology. 2006 Jan 16;3(1):7
  15. PMID 34586875
    .
  16. S2CID 6150236
    .
  17. PMID 17727910
    .
  18. PMID 18060323
    .
  19. PMID 18054325
    .
  20. PMID 18688285
    .
  21. PMID 17971877
    .
  22. S2CID 14519920. {{cite book}}: |journal= ignored (help
    )
  23. PMID 17487374
    .
  24. ^
    PMID 11818490
    .
  25. PMID 9360927
    .
  26. PMID 10749578
    .
  27. PMID 10500107
    .
Retrieved from "https://en.wikipedia.org/w/index.php?title=Virus_latency&oldid=1198599968"