Modulation of cellular tropism and innate antiviral response by viral glycans.

Arthropod-borne viruses (arboviruses) are a significant cause of human and animal disease worldwide. Multiple interactions between virus and the host innate immune system ultimately determine the pathogenesis and clinical outcome of the infection. Evidence is rapidly emerging that suggests viral glycans play a key role in viral pathogenesis by regulating host cell tropism and interactions with the host innate immune response.

Ross River virus envelope glycans contribute to type I interferon production in myeloid dendritic cells.

Alphaviruses are mosquito-transmitted viruses that cause significant human disease, and understanding how these pathogens successfully transition from the mosquito vector to the vertebrate host is an important area of research. Previous studies demonstrated that mosquito and mammalian-cell-derived alphaviruses differentially induce type I interferons (alpha/beta interferon [IFN-alpha/beta]) in myeloid dendritic cells (mDCs), where the mosquito cell-derived virus is a poor inducer of IFN-alpha/beta compared to the mammalian-cell-derived virus. Furthermore, the reduced IFN-alpha/beta induction by the mosquito cell-derived virus is attributed to differential N-linked glycosylation.

In vivo experimentation with simian herpesviruses: assessment of biosafety and molecular contamination.

In vivo studies with highly pathogenic viruses prompt concerns regarding the persistence of infectious virus in pathology specimens. Although formalin fixation of tissues may inactivate infectious virus, fixation may also degrade viral nucleic acid and antigens, thereby limiting detection of virus in tissues by polymerase chain reaction (PCR) amplification or immunohistochemistry (IHC). We sought to: 1) assess the rate of inactivation of infectious virus in tissue specimens during formalin fixation, 2) assess IHC recognition of viral antigens and PCR detection of viral DNA after long-term (14 d) formalin fixation, and 3) investigate microtome contamination by DNA carry-over to subsequently sectioned tissues.

A naturally occurring fatal case of Herpesvirus papio 2 pneumonia in an infant baboon (Papio hamadryas anubis).

Here we describe the unusual finding of herpesvirus pneumonia in a 7-d-old infant baboon (Papio hamadryas anubis). This animal had been separated from its dam the morning of its birth and was being hand-reared for inclusion in a specific pathogen-free colony. The baboon was presented for anorexia and depression of 2 d duration.

Neuropathogenesis of herpesvirus papio 2 in mice parallels infection with Cercopithecine herpesvirus 1 (B virus) in humans.

Cercopithecine herpesvirus 1 (monkey B virus; BV) produces extremely severe and usually fatal infections when transmitted from macaque monkeys to humans. Cercopithecine herpesvirus 16 (herpesvirus papio 2; HVP2) is very closely related to BV, yet cases of human HVP2 infection are unknown. However, following intramuscular inoculation of mice, HVP2 rapidly invades the peripheral nervous system and ascends the central nervous system (CNS) resulting in death, very much like human BV infections.

Experimental infection of baboons (Papio cynocephalus anubis) with apathogenic and neurovirulent subtypes of herpesvirus papio 2.

Cercopithecine herpesvirus 16 (Herpesvirus papio 2; HVP2) is an alpha-herpesvirus of baboons (Papio spp.) that generally causes minimal to inapparent disease in the natural host species. HVP2 is very closely related genetically and antigenically to Cercopithecine herpesvirus 1 (monkey B virus; BV) of macaques, which is well known for its extreme lethality in nonmacaque species including humans.

Alternate circulation of recent equine-2 influenza viruses (H3N8) from two distinct lineages in the United States.

Phylogenetic and antigenic analyses indicate that recent circulating equine-2 influenza viruses in the United States have been alternating between two genetic and antigenic distinct lineages since 1996. The evolution rates for these two lineages, the Kentucky and the Florida lineage, are very similar. For the earlier isolates in the Kentucky lineage, there are multiple and sequential nonsynonymous substitutions at antigenic sites B and D.

Pathogenicity of different baboon herpesvirus papio 2 isolates is characterized by either extreme neurovirulence or complete apathogenicity.

In comparisons of the pathogenicity of simian alphaherpesviruses in mice, two isolates of the baboon virus HVP2 were nearly as lethal as monkey B virus, a biological safety level 4 agent (J. W. Ritchey, K.