ABSTRACT
EBV-associated malignancies remain a considerable problem in HIV-infected individuals, even in the era of HAART. Although EBV is a common factor, each disease has a unique pathogenesis. Study of these diseases reveals the viral proteins expressed in the malignancies that might contribute to the development of the disease as well as the molecular basis for pathogenesis. It is likely that this knowledge will contribute to the development of novel therapeutics that will result in more favorable outcomes in the future.
Subject(s)
Acquired Immunodeficiency Syndrome/complications , Epstein-Barr Virus Infections/complications , Herpesvirus 4, Human/physiology , Herpesvirus 4, Human/genetics , Herpesvirus 4, Human/isolation & purification , Humans , Neoplasms/pathology , Neoplasms/virology , Virus LatencyABSTRACT
A virus, designated Rana catesbeiana virus Z (RCV-Z), was isolated from the visceral tissue of moribund tadpoles of the North American bullfrog Rana catesbeiana. SDS-PAGE (sodium dodecyl sulfate polyacrylamide gel electrophoresis) analysis of viral proteins and sequence analysis of the amino terminal end of the major capsid protein showed that RCV-Z was similar to frog virus 3 (FV3) and other ranaviruses isolated from anurans and fish. However, analysis of restriction fragment profiles following digestion of viral genomic DNA with XbaI and BamHI indicated that RCV-Z was markedly different from FV3. Moreover, in contrast to FV3, RCV-Z contained a full-length copy of the viral homolog of eukaryotic initiation factor 2 alpha (eIF-2alpha). Experimental infection of bullfrog tadpoles with FV3 and RCV-Z demonstrated that RCV-Z was much more pathogenic than FV3, and that prior infection with FV3 protected them from subsequent RCV-Z induced mortality. Collectively, these results suggest that RCV-Z may represent a novel species of ranavirus capable of infecting frogs and that possession of a viral eIF-2alpha homolog (vIF-2alpha) correlates with enhanced virulence.