A 36-bp deletion close to the 5' end of NEF that impaired Nef function was found in a long-term nonprogressor with human immunodeficiency virus type 1 (HIV-1) infection. Forms containing an adjacent duplication of 33 bp were also frequently observed. The duplication showed no homology to the deleted region but restored the overall length of the first variable loop of Nef. NEF alleles carrying the duplication were active in class I major histocompatibility complex (MHC-I) down-modulation and enhancement of virus infectivity. However, they showed little activity in CD4 down-regulation and were unable to stimulate viral replication in human peripheral blood mononuclear cells. Our study indicates that the enhancement of virion infectivity and the stimulation of HIV-1 replication in lymphocytes are distinct functions of Nef. Our findings also illustrate the capacity for repair of attenuating deletions in HIV-1 infection and suggest that a selective pressure for Nef-mediated MHC-I down-modulation and/or enhancement of virion infectivity exists.

We describe a case of aggressive Bartonella henselae endocarditis in an immunocompetent man who owned a cat. Aortic valve replacement was required, and his infection was diagnosed by histology, serology, and polymerase chain reaction analysis. The manifestations of his disease included mediastinal lymphadenopathy, glomerulonephritis, myocarditis, and a petechial rash; the unusual finding of a positive titer of c-antineutrophil cytoplasmic antibodies was noted. Serological titers were markedly elevated for > 1 year despite clinical improvement.