No abstract

Human polyomavirus BK (BKV) and JC (JCV) infections were examined in persons infected with human immunodeficiency virus type 1 (HIV-1). High frequencies of BKV (24%) and JCV viruria (16%) were detected by polymerase chain reaction (PCR). BKV viruria was not found in an immunocompetent control group, in contrast to a frequency of JCV viruria of 20%. The degree of HIV-induced immunodeficiency did not influence the prevalence of BKV viruria, in contrast to cytomegalovirus viruria, suggesting BKV reactivation is an early manifestation in HIV infection as well as a temporal sequence of opportunistic infections. BKV DNA but not JCV DNA was detected in peripheral blood mononuclear cells (PBMC) in 2 of 42 subjects by a sensitive nested PCR. Sequencing of viral noncoding control regions (NCCRs) revealed predominantly archetypal and TU type BKV NCCRs but only archetypal JCV NCCRs. A new, naturally occurring BKV NCCR variant was detected in 1 urine specimen and 2 PBMC samples, indicating a stable and biologically significant rearrangement. Serum levels of BKV antibodies do not seem to be diagnostically useful in HIV-infected persons.

Ficolin-3, encoded by the FCN3 gene and expressed in the lung and liver, is a recognition molecule in the lectin pathway of the complement system. Heterozygosity for an FCN3 frameshift mutation (rs28357092), leading to a distortion of the C-terminal end of the molecule, occurs in people without disease (allele frequency among whites, 0.01). We describe a patient with recurrent infections who was homozygous for this mutation, who had undetectable serum levels of ficolin-3, and who had a deficiency in ficolin-3-dependent complement activation.

Campylobacter concisus has been as frequently isolated from human diarrhea as the important enteropathogen Campylobacter jejuni, but it also occurs in the feces of healthy individuals. The role of C. concisus in human disease has been difficult to determine, since the species comprises at least two phenotypically indistinguishable but genetically distinct taxa (i.e., genomospecies) that may vary in pathogenicity. We examined 62 C. concisus strains by amplified fragment length polymorphism (AFLP) profiling and correlated the results with clinical data. All C. concisus strains gave unique AFLP profiles, and numerical analysis of these data distributed the strains among four clusters. The clustering was of taxonomic significance: two clusters contained, respectively, the type strain (of oral origin) and a reference strain (from diarrhea) of each of the known genomospecies. Genomospecies 2 strains were more frequently isolated from immunocompetent patients and/or patients without concomitant infections that presented with fever, chronic diarrhea, and gut inflammation than was genomospecies 1, clustering with the type strain of oral origin. Bloody diarrhea was recorded only with C. concisus genomospecies 2 infections. We identified two additional C. concisus genomospecies: genomospecies 3 comprised a single strain from an immunocompetent patient, and genomospecies 4 contained five isolates from severely immunodeficient patients, i.e., organ transplantation recipients or those with hematological malignancies. All genomospecies 4 strains were of the same protein profile group and failed to react with a C. concisus species-specific PCR assay based on 23S rRNA gene sequences: the taxonomic position of this group requires closer investigation. Campylobacter concisus is genetically and taxonomically diverse and contains at least four distinct genomospecies that may exhibit differences in their spectra of virulence potential.