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Figure 11.4. Overall view of BVDV infection, replication, and release of progeny virus derived using currently available information. Please see text for additional details.
membrane, releasing the virus particle into the extracellular environment. The budding of the capsidbound genomic RNA and the immature virus particle into the lumen of the endoplasmic reticulum, followed by the release of mature particles directly from a vesicle fused with the plasma membrane, would explain why viral antigens are not found associated with plasma membrane of the infected cell.
FINAL REMARKS
Replication of an RNA virus in a susceptible cell is a complicated affair, requiring essentially all of the cell’s resources. This is an intricate combination of cellular machinery and virus-encoded proteins working in concert, most often to the detriment of the cell, to bring about production of progeny virus. Some of these effects are obvious, but others are very subtle in their effect. Increasingly more experimental evidence is available showing the dependence on host cell proteins in carrying out many aspects of virus replication. BVDV is no different, although much of what we know is supported or inferred from work with other pestiviruses or flaviviruses. Regardless, much is left to do. This is par-
ticularly true in two areas. The first is how the virus interacts with the host cell in establishing a chronic infection in utero that results in the birth of a persistently infected calf. The second is the subtle interactions with the host immune system and how it is manipulated to delay both the innate and acquired immune responses. Continued work will give greater insight into replication strategy of pestiviruses and possible means to intervene, yielding better vaccination strategies and perhaps pharmacological treatments to prevent, inhibit, or moderate infection.
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