Bunyavirus - Replication, Pathogenesis
Replication of Bunyavirus
Replication of Bunyavirus occurs in the cytoplasms of the host cells.
In some phleboviruses, the small RNA segment is ambisense (i.e., one portion is viral complementary in sense and another portion is viral in sense).
Genetic reassortment can occur during infection because the RNA is segmented.
Virus particles bud into the Golgi cisternal and are liberated from the cell by plasma membrane disruption and by fusion of intracellular vacuoles with the plasma membrane.
Pathogenesis of Bunyavirus
Except for members of the genus Hantavirus, bunyaviruses replicate in arthropods. The gut of the vector is infected initially, and after a few days or weeks, the virus appears in the saliva- the arthropod then remains infective for life but is not ill. When the vector takes a blood meal, the infective saliva enters the small capillaries or lymphatics of the human or other vertebrate hosts.
The primary site of bunyavirus replication in humans is not known- it may be the vascular endothelium, the skin, or the regional lymph nodes. An incubation period is around a few days ensures, after which the vertebrate host develops viremia.
The bunyavirus infection is usually apparent less often, and the host becomes febrile, manifesting the more serious signs and symptoms that are characteristic of infecting a virus. Viremia subsides with the appearance of humoral Ab, and the host recovers unless a specific target organ is affected.
The target organs include the liver in Right valley fever, the brain in La Crosse encephalitis, the liver and vascular endothelium in Crimean-Congo hemorrhagic fever and hemorrhagic fever with renal syndrome, and the lung in hantavirus pulmonary syndrome is damaged and specific disease occurs.
Although the damage in most infections is believed to result from direct invasion by the virus and not from a host-mediated Ag-Ab or Ag lymphocyte reaction, the pathogenesis of bunyaviruses in the vertebrate host has not been extensively studied.
The damage to the kidneys in hemorrhagic fever with renal syndrome and to the brain and retina in Rift Valley fever occurs after humoral Ab is formed. These complications have been postulated to result from a host reaction.
Steps in development of pathogenesis of Bunyavirus
Via bite of mosquito/arthropod vector virus reacts small blood capillaries or lymphatics
The primary site of infection is not known but may be a regional lymph node, skin, endothelium
After the Incubation Period of a few days, uremia occurs
Usually asymptomatic but in both cases may cause febrile illness along with serious symptoms depending upon the type of virus infecting
Viremia subsides with the development of Humoral Ab unless the target organ is infected
Organs involved:
La Crosse encephalitis => brain
Crimean-Congo hemorrhagic fever with renal syndrome => liver, kidney, vascular endothelium
Rift Valley fever => liver, brain, retina
Hantavirus pulmonary syndrome => lungs
Damage is believed due to the invasive nature and extensive replication of the virus not because of host immune responses (Ag-Ab reaction/Ag- lymphocyte reaction)