Abstract
The course of viral infections can be influenced by a variety of host factors as well as by co-infection of the host with one or more other viruses. Studies in cells co-infected with the human immunodeficiency virus (HIV) and a second virus have demonstrated transactivation of transcription from the HIV LTR by products of the second virus. Several classes of viruses, including papovaviruses (6), herpesvirus (8, 13, 15) and hepatitis B virus (23) have been shown to have this transactivating property. A second virus can also activate transcription of HIV proviruses by indirect mechanisms, such as by inducing the transcription factor NFkB, which acts on the HIV LTR (14). The human T cell leukemia viruses (HTLV-I and HTLV-II) may enhance HIV replication by a different means; HTLV particles have a direct mitogenic effect on T cells (possibly by binding to a cell surface growth factor receptor) and thus stimulating production of HIV from infected T cells (5, 28).
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