Field isolates of foot-and-mouth disease virus (FMDV) have been shown to use the RGD-dependent integrin ␣v3 as a cellular receptor on cultured cells. However, several other RGD-dependent integrins may have the potential to act as receptors for FMDV in vivo. Of these, ␣v6 is a likely candidate for use as a receptor by FMDV as it is expressed on epithelial cells, which correlates with the tissue tropism of the virus. In this report, we show that human colon carcinoma cells (SW480) that are normally nonpermissive for FMDV become susceptible to infection as a result of transfection with the integrin 6 subunit and expression of ␣v6 at the cell surface. Integrin ␣v6 is the major site for virus attachment on the 6-transfected cells, and binding to ␣v6 serves to increase the rate of virus entry into these cells. In addition, we show that virus binding and infection of the 6-transfected cells is mediated through an RGD-dependent interaction that is specifically inhibited by a monoclonal antibody (10D5) that recognizes ␣v6. These studies establish a role for ␣v6 as a cellular receptor for FMDV.
To understand the mechanisms involved in protective immunity to African swine fever virus (ASFV) infection, the observation that infection with the avirulent Portuguese ASFV isolate OUR/T88/3 protects outbred pigs from challenge with the virulent Portuguese ASFV isolate OUR/T88/1 was exploited. It was demonstrated that pigs exposed to OUR/T88/3 and then depleted of CD8 + lymphocytes were no longer fully protected from OUR/T88/1 challenge. This indicated that CD8 + lymphocytes play an important role in the protective immune response to ASFV infection and that anti-ASFV antibody alone, from OUR/T88/3 infection, was not sufficient to protect pigs from OUR/T88/1 challenge. Inbred pigs of the cc haplotype infected with OUR/T88/3 were not always protected from OUR/T88/1 challenge and developed both viraemia and fever. Such viraemia was always correlated with increased numbers of circulating CD8b + lymphocytes, indicating a specific role for CD8b + lymphocytes in combating viraemia. These experiments indicate an important role for CD8 + lymphocytes, particularly CD8b + lymphocytes, in ASF protective immunity.
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