- Volume 70, Issue 2, 1989

Infection of chickens by a virulent avian influenza A virus, A/turkey/Ont/7732/66 (H5N9), was associated with a severe lymphopenia. High titres of infectious virus were found in lymphoid tissues early in infection and were accompanied by severe damage to the lymphocyte populations as demonstrated by histopathological examination. Non-lymphoid cell populations in these tissues were unaffected, as were other organs examined. The viral nucleoprotein was localized by immunoperoxidase staining to lymphocytes in affected tissues early in infection.

SJL/J mice are resistant, whereas A/WySnJ mice are susceptible to intraperitoneally (i.p.) inoculated street rabies virus (SRV). In this report we determine whether interferon (IFN) induced within the central nervous system (CNS) of these mice during infection is associated with resistance. We show that the high concentration of type 1 interferon (IFN-α/β) within the CNS of A/WySnJ mice is ineffective in inhibiting SRV replication in these tissues, and is unimportant in ameliorating disease. More importantly, the 100% survival of SRV-infected SJL/J mice following neutralization of IFN within the CNS with anti-IFN-α/β suggests that protection of target cells by this minimal amount of IFN is not the mechanism responsible for the innate resistance of SJL/J mice to i.p. inoculated SRV.

We report the isolation of human immunodeficiency virus type 2 (HIV-2) from each of six West Africans with AIDS-related complex or AIDS. One isolate (HIV-2 cam2) was molecularly cloned and shown by restriction mapping to differ in seven out of 22 sites from the prototype HIV-2 rod . Nevertheless, by a number of serological criteria these isolates are all clearly HIV-2.

We have compared detailed physical maps of the genomes of four capripoxvirus isolates, representing four capripoxvirus genome types. The comparisons strongly suggest that the progenitor of one of these isolates arose by genetic recombination between members of two of the other three types.

Mutants of African cassava mosaic virus containing extensive deletions across the coat protein gene that remove up to one-third of the genomic component have been constructed and shown to be infectious when mechanically inoculated onto Nicotiana benthamiana by leaf abrasion. Using N. tabacum protoplasts we demonstrate that mutant pCLV. CPΔ11, containing a 712 bp deletion, is competent for replication in its deleted form. However, systemic spread of pCLV. CPΔ11 and other deletion mutants is associated with reversion of DNA 1 to a size comparable to that of the native genomic component. This contrasts with the behaviour of coat protein mutants of the closely related geminivirus tomato golden mosaic virus which maintain their deletions during spread. Appraisal of the different inoculation procedures used to introduce the mutants into plants suggests the imposition of a stringent size requirement for localized cell-to-cell spread which is relaxed for long distance spread through the vascular system.

Three spontaneous mutants of strain TpM-34 of red clover necrotic mosaic virus, designated M-A, M-B and M-C, were isolated. In gel diffusion tests the three mutants were serologically indistinguishable from the parent but when inoculated onto Vigna unguiculata each induced characteristic symptoms which differed from those induced by TpM-34. TpM-34 induced similar numbers of lesions at 17 °C and 26 °C. However, although inoculation with RNA of the mutants induced 70 to 80% as many lesions as inoculation with TpM-34 RNA at 17 °C, very few lesions were induced by any of the mutants at 26 °C. The symptoms induced by heterologous mixtures of RNA 1 or RNA 2 of TpM-34 with RNA 2 or RNA 1 of each mutant indicated that M-A, M-B and M-C each has mutations in both RNA components, but that symptom expression was determined predominantly by RNA 1.

The complete nucleotide sequence (2217 residues) of RNA 3 of cucumber mosaic virus strain O (CMV-O) was determined. Two open reading frames were identified, encoding a 3A protein (279 amino acid residues) in the 5′-proximal region and a coat protein (218 amino acid residues). The amino acid sequence of the coat protein C terminus was determined directly from purified protein, and confirmed the presence of the coat protein open reading frame in CMV-O RNA 3. Comparison of nucleotide sequences and amino acid sequences of CMV strains O, Q, D and Y indicated the close relationship between these strains. A tRNA-like structure could be adopted by the 3′ non-coding region, and this resembled a similar structure in CMV-Q in spite of nucleotide substitutions or deletions.