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Category: Clinical Microbiology
Bovine Viral Diarrhea Virus in Mixed Infections, Page 1 of 2
< Previous page | Next page > /docserver/preview/fulltext/10.1128/9781555817947/9781555812447_Chap03-1.gif /docserver/preview/fulltext/10.1128/9781555817947/9781555812447_Chap03-2.gifAbstract:
Bovine viral diarrhea virus (BVDV) is classified in the Pestivirus genus within the Flaviviridae family, which also contains the Flavivirus and Hepacivirus genera. Infection of cattle with BVDV induces three disease conditions that range from clinically inapparent to clinically severe. The conditions are termed as congenital persistent infection, mucosal disease, and acute bovine viral diarrhea (BVD). Mucosal disease is a sequel of congenital persistent infection and is caused by a “mixed” infection of noncytopathic BVDV and cytopathic BVDV. Acute BVD occurs after birth and is induced by primary postnatal infection with either cytopathic or noncytopathic BVDV. Acute BVDV may result in respiratory, enteric, and/or reproductive disease. The severity of disease varies from clinically inapparent to fatal and depends on the virulence of the viral strain, physical and environmental stressors, and intercurrent infection with other pathogens. During acute or persistent infection with BVDV, viral replication occurs in a variety of cell types located in the integument, alimentary canal, nervous system, respiratory tract, and immune system. Although many cell types are permissive for viral replication, BVDV has a predilection for cells of the immune system. Viral replication in lymphoid cells may directly, or indirectly, alter immune function and enhance severity of disease during mixed infections of BVDV or mixed infections of BVDV with other pathogens. This chapter provides examples of mixed infections involving BVDV, and discusses the role BVDV may have in enhancing disease processes during a mixed infection.
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The genomic organization of BVDV. The pestivirus genomic RNA lacks a 5΄ cap and 3΄ poly(A) tail. The long 5΄-untranslated region (UTR) has an internal ribosome entry site for initiation of translation. The viral structural proteins are named C (the capsid protein), Erns, E1, and E2. (The last three proteins are in the viral envelope.) Viral-neutralizing antibody reacts primarily with E2, but some viral-neutralizing antibody reacts with Erns. Antigenic similarity between BVDV usually is assessed by using monoclonal or polyclonal antibody against E2. Both noncytopathic BVDV and cytopathic BVDV produce the nonstructural protein NS2-3. However, the NS2-3 protein of cytopathic BVDV is cleaved to form the NS-2 and NS-3 proteins. Expression of the NS3 protein is considered the molecular marker for cytopathic BVDV (see references 53 , 90 , and 117 ).
The genomic organization of BVDV. The pestivirus genomic RNA lacks a 5΄ cap and 3΄ poly(A) tail. The long 5΄-untranslated region (UTR) has an internal ribosome entry site for initiation of translation. The viral structural proteins are named C (the capsid protein), Erns, E1, and E2. (The last three proteins are in the viral envelope.) Viral-neutralizing antibody reacts primarily with E2, but some viral-neutralizing antibody reacts with Erns. Antigenic similarity between BVDV usually is assessed by using monoclonal or polyclonal antibody against E2. Both noncytopathic BVDV and cytopathic BVDV produce the nonstructural protein NS2-3. However, the NS2-3 protein of cytopathic BVDV is cleaved to form the NS-2 and NS-3 proteins. Expression of the NS3 protein is considered the molecular marker for cytopathic BVDV (see references 53 , 90 , and 117 ).
Origin of cytopathic BVDV in cattle persistently infected with noncytopathic BVDV, form of mucosal disease induced, production of virus-neutralizing antibody, and viral isolation post mortem
Origin of cytopathic BVDV in cattle persistently infected with noncytopathic BVDV, form of mucosal disease induced, production of virus-neutralizing antibody, and viral isolation post mortem