The pathogenesis of arbovirus infections, in this case due to members of the bunyavirus genus, is different from that of other viral dlseases because transmission through an invertebrate host is essential to maintaln the infectious cycle. This requires that these viruses must be capable of replication in both vertebrates and invertebrates. Additionally, the preferred hosts of the vector play a role in determining which vertebrate hosts are ultimately infected by these viruses. For the serogroups discussed several patterns emerge . For members of the Bunyamwera serogroup the major vertebrate host appear to be humans and domestic ani- mals. For group C viruses the hosts include humans, rodents, and marsupials. The host animals for the California serogroup seem well defined with the major ones being humans and small forest mammals with some ungulates involved. Mosquitoes are the major invertebrate host for these 3 serogroups. Those viruses of the Simbu serogroup which infect animals seem to infect introduced domestic animals species and have one Culicoides species (midge) as the major invertebrate host, whereas ORO, that virus within the serogroup infecting humans, appears to occur in 2 cycles of transmission, an urban cycle and a sylvatic cycle, one involving Culicoides.
Once the vertebrate host is inoculated, vims replication occurs at or near the site of entry and is followed by the development of a viremia. This viremia, although of short duration, transfers infectious virus to the blood-brain barrier or the placental junction. Virus infection at these sites must then occur before invasion of the central nervous system or fetus respectively can occur. Viruses from the different serogroups show very different host cell specificities. Viruses of the Bunyamwera and California serogroups exhibit a tropism for the endothelial cells forming the barrier of the central nervous system and subsequently infect various areas of the central nervous system whereas viruses of the Simbu serogroup appeared to infect the endothelial cells associated with the placental junction, subsequently the cells of the trophoblast and finally the developing fetus.
The techniques used thus far in studying viral infection and transport to speciflc organs and/or tissues have included gross pathology (which only identifies an infection once damage to cellular tissue has occurred), titration of virus (this indicates the amount of infectious virus in the whole tissue or organ examined), and fluorescent or immunochemical techniques. These latter techniques are the most definitive procedures for identifying viral antigens within cells. The fluorescent antibody technique only detects substantial quantities of viral antigen. Newer histochemical techniques using avidin-biotin binding and enzymes such as horseradish peroxidase and glucose oxidase are proving more sensitive in the detection of viral antigen. Detection of viral specifIc nucleic acid is now possible using in situ hybridization techniques which are extremely sensitive and can detect as few as 10 viral genomes per infecte cell (Brahic et al., 1984). Thus both viral nucleic acid and viral proteins (antigen) can be detectad in infected cells.
Studies of the structure and function of viral proteins and nucleic acids for members of the bunyavirus genus have uncovered the importance of the viral surface structural proteins G1 and/or G2 coded for by the M RNA gene. These surface glycoprotein spikes play a critical role in viral pathogenesis as one or both appear to be involved in viral attachment and possibly penetration and subsequent virus replication in a susceptible host cell. In vitro studies of selected neuronal and placental cell subpopulations may assist in determining which cell populations are involved in viral infection in vivo and the resultant pathogenesis.