Arbovirus enter cells by receptor-mediated endocytosis and exit by budding from
the plasma membrane.
Arbo viruses enter the body via mosquito bites and replicate in various tissues,
including Langerhans cells, which then migrate to lymph nodes, causing viremia.
Viremia results in invasion of the central nervous system (CNS) by arbovirus that
cause encephalitis and meningitis or of the joints and internal organs by viruses that cause fever,
arthralgia, and rash.
All arbovirus suppress the innate immune response by inhibiting JAK/STAT
signaling, a major early determinant of disease severity.
At later times, recovery is mediated by virus-neutralizing antibodies and cytotoxic T cells.
The viruses are capable of boosting the immune system of the host cell and aids in the production of interferons.
Ebola virus enters the patient through mucous membranes, breaks in the skin, or parenterally and following cells are gets infected.
The cells might include monocytes, macrophages, dendritic cells, endothelial cells, fibroblasts, hepatocytes, adrenal cortical cells, and epithelial cells.
The incubation period may be related to the infection route (6 days for injection versus 10 days for contact).
Ebola virus moves from the initial infection site to regional lymph nodes and might subsequently passes to the liver, spleen, and adrenal gland.
Although not infected by Ebola virus, lymphocytes undergo apoptosis resulting in decreased lymphocyte counts.
Hepatocellular necrosis occurs and is associated with dysregulation of clotting factors and subsequent coagulopathy.
Adrenocortical necrosis also can be found and is associated with hypotension and impaired steroid synthesis.
Ebola virus appears to trigger a release of pro-inflammatory cytokines with subsequent vascular leak and impairment of clotting ultimately resulting in multiorgan failure and shock