Laboratory-acquired vaccinia infection

Abstract Background: Complications following vaccination with vaccinia virus have been well described but are not commonly observed. The use of vaccinia as a tool in molecular biology, in the development of therapeutics, and the anticipated increase of vaccinations in the general population due to the threat of bioterrorism have created a renewed awareness of the post-vaccination complications and the consequent need for clinical and laboratory diagnosis. Objectives: To report the clinical presentation and subsequent diagnosis of generalized vaccinia that resulted from a laboratory accident in an unvaccinated subject. Study design: The patient was seen by a local infectious disease's specialist and evaluated clinically and with laboratory support relative to a differential diagnosis. Results: Careful assessment of the patient's history, an evaluation of the workplace, and the elimination of likely microbial etiologies led to the diagnosis of generalized vaccinia. Laboratory confirmation was obtained by use of electron microscopy (EM) to observe poxvirus particles in infected cell cultures. Conclusions: Exposure to vaccinia virus should raise the index of suspicion for patients with skin lesions. Rapid diagnosis may be accomplished by direct examination of lesion material by EM. The virus also readily replicates in commonly available cell cultures and in the absence of immune reagents, typical poxvirus particles may be observed in the infected cells by EM

The major genetic determinants of HIV-1 control affect HLA class I peptide presentation.

Infectious and inflammatory diseases have repeatedly shown strong genetic associations within the major histocompatibility complex (MHC); however, the basis for these associations remains elusive. To define host genetic effects on the outcome of a chronic viral infection, we performed genome-wide association analysis in a multiethnic cohort of HIV-1 controllers and progressors, and we analyzed the effects of individual amino acids within the classical human leukocyte antigen (HLA) proteins. We identified >300 genome-wide significant single-nucleotide polymorphisms (SNPs) within the MHC and none elsewhere. Specific amino acids in the HLA-B peptide binding groove, as well as an independent HLA-C effect, explain the SNP associations and reconcile both protective and risk HLA alleles. These results implicate the nature of the HLA-viral peptide interaction as the major factor modulating durable control of HIV infection