Viral pathogenesis

Viral pathogenesis is the study of how biological viruses cause diseases in their target hosts, usually carried out at the cellular or molecular level. It is a specialized field of study in virology.[1] Pathogenesis is a process in which an initial infection becomes a disease.[2] Viral disease is the sum of the effects on the host caused by the replication of the virus and of the host's subsequent immune response.[3] Viruses are able to initiate infection, disperse throughout the body, and replicate due to virulence characteristics.[4] Mechanisms of pathogenesis of viral diseases include: implantation of the virus at the portal of entry, local replication, spread to target organs, and shedding of the virus into the environment. There are several factors that affect pathogenic mechanisms. Some of these factors include virulence characteristics of the virus that is infecting. In order to cause disease, the virus must overpower several inhibitory effects present in the host. Some of the inhibitory effects include distance, physical barriers, host defenses, and conflicting cellular susceptibilities. These inhibitory effects may differ among individuals and different races due to the inhibitory effects being genetically controlled.

Mechanisms of Infection

Three requirements must be satisfied to ensure a successful infection of a host. There must be sufficient virus available to initiate the infection. Cells at the site of infection must be accessible, susceptible, and allow the virus to enter, and the host anti-viral defense systems must be ineffective or absent.[3]

There are several mechanisms that must occur for a viral disease to develop:[2]

  • Implantation at Portal of Entry: The virus must implant at the entry portal into the body. Implantation is the earliest stage of pathogenesis. Implantation frequency is at its greatest where viruses directly contact living cells. Viruses usually implant on cells of respiratory, gastrointestinal, skin and genital tissues. Some viruses are capable of implanting in a fetus through infected germ cells at the time of fertilization. Implantation can also occur later in the pregnancy via the placenta, and also at birth. There are several factors that may affect the end result of the infection. The virulence of the virus and implantation point are a couple of factors that impact the severity of the disease.[4]
  • Local Replication and Local Spread: Local replication and spread of the virus follows implantation. Replicated virus from the initially infected cell has the capability to disperse to neighboring extracellular fluids or cells. Spread occurs by the neighboring cell being infected or the virus being released into extracellular fluid.[4]
  • Replication: The invading virus must reproduce itself in large numbers. It usually does this intracellularly.
  • Dissemination in Nerves: The spread of virus through the nerves is less common than the spread through the bloodstream.[4]
  • Dispersal: The replicated viruses must spread to target organs (disease sites) throughout the body. The most common route of spread from the portal of entry is the circulatory system, which the virus reaches via the lymphatic system. Viruses can access target organs from the blood capillaries by multiplying inside endothelial cells, moving through gaps, or by being carried inside the organ on leukocytes. Some viruses, such as Herpes,[5] rabies and polio viruses, can also disseminate via nerves.
  • Shedding: The viruses must spread to sites where shedding into the environment can occur. The respiratory, alimentary and urogenital tracts and the blood are the most frequent sites of shedding.

Factors that Affect these Pathogenic Mechanisms are:[2]

  • How accessible the host tissues are to the virus: The degree to which the tissues of the body and organs are accessible. Accessibility is affected by physical barriers (for example: tissue barriers and mucus). It is also impacted by the distance to be traveled through the body and by the natural defense mechanisms.[2]
  • How susceptible the host cells are to virus multiplication: Infection is only capable of occurring if virus replicating cells are present. Cellular susceptibility needs a receptor for the virions and an intracellular environment that allows the virus to replicate and release.[2]
  • Whether the virus is susceptible to the host's defenses: Host defenses may inhibit replication. To be able to cause disease, the virus needs to be able to overcome the preventative effects of physical barriers, host defenses, and contradicting cellular susceptibilities to infection.[2]

Incubation Period

Viruses that travel a short distance to reach their target organ have a short incubation period. The incubation period tends to be 1 to 3 days. On the other hand, with generalized infections, the incubation period is longer because of how long it takes the virus to move throughout the body and reach the target organs. There are several other factors that affect the incubation period. The mechanisms behind long incubation periods, months or years for example, are not completely understood yet.

Evolution

As with all parasites, natural selection favors the development of low-virulence virus strains.[2] When a pathogen first invades a new host species, the hosts have little or no immunity and often suffer high mortality. Those that survive do so because they have different genetics that offer them some protection from the new pathogen. These survivors then reproduce and pass on those genes, resulting in lower mortality rates in future generations. There is no advantage to a pathogen to kill the host before dispersal to new hosts, thus a decrease in virulence over time is usually observed.

See also

References

  1. ↑ Nathanson, Neal. Viral pathogenesis. Lippincott-Raven. p. 1997. ISBN 9780781702973.
  2. 1 2 3 4 5 6 7 S Baron; M Fons; T Albrecht, eds. (1966). Medical Microbiology Chapter 45 Viral Pathogenesis (6 ed.). |access-date= requires |url= (help)
  3. 1 2 Racaniello, Vincent. "Viral Pathogenesis" (PDF). Retrieved 8 February 2014.
  4. 1 2 3 4 Baron, Samuel; Fons, Michael; Albrecht, Thomas (1996). Baron, Samuel, ed. Medical Microbiology (4th ed.). Galveston (TX): University of Texas Medical Branch at Galveston. ISBN 0963117211. PMID 21413306.
  5. ↑ http://www.herpes-coldsores.com/std
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