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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. Pathogenesis is a process in which an initial infection becomes a disease. Viral disease is a sum of the effects on the host caused by the replication of the virus and of the host's subsequent immune response. copied from Viral pathogenesis. Mechanisms of pathogenesis of viral diseases include: Implantation of virus at the portal of entry, local replication, spread to target organs, spread to sites of shedding of 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 should overpower several inhibitory effects. 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. Viruses are able to initiate infection, disperse throughout the body, and replicate due to virulence characteristics.

Mechanisms of Infection: - 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.

-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 or intracellular cells. Spread to extracellular cells transpires by the neighboring cell being infected or the virus being released into extracellular fluid.

-Circulation in the Bloodstream from the Portal of Entry:

-Dissemination in Nerves: The spread of virus through the nerves is less common than the spread through the bloodstream.

-Shedding of Virus: All sites of shedding are utilized because viruses are so diverse. Incubation Period: With viruses that travel a short distance to reach their target organ, therefore; the incubation period is often of short duration. The incubation period tends to be 1 to 3 days. On the other hand, with generalized infections, the incubation period is often longer because of how long it takes the virus to move throughout the body and reach the target organ. 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.

Multiplication in Target Organs:

Factors that Affect these Pathogenic Mechanisms are:

 * How accessible the host tissues are: 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.
 * 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.
 * 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.