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Visually explore Herpes Simplex Virus 1 pictures, or more commonly known asĀ Oral Herpes (cold sores) Pictures. We have known for a long time that strains of HSV-1 are genetically variable, and new deep sequencing approaches allow us to fully define these differences and begin to understand how they affect phenotype.
We would like to better understand how HSV latency affects the host neuron and its neighboring cells. While vaccines have largely defeated the paralysis caused by polio, other viruses such as rabies, West Nile virus, and herpes simplex virus (HSV) continue to cause neurological infections that require clinical intervention. For example, previous work has shown that attenuated strains of HSV-1 do not replicate well in the nervous system, causing little disease in animal models. In lab experiments, HSV infection of neurons has been associated with changes in neuropeptide release, neuronal firing rates, axon remodeling, and interferon production.

Previous tools to map differences between HSV strains included restriction digest mapping or candidate-gene approaches.
While neurons are not specialized for immune control or attack, they do contain intrinsic cellular defenses. Now we can readily sequence the full genomes of many strains, use bioinformatics to associate variations with virulence phenotypes, and then test these genetic associations experimentally. Although not all of those infected experience noticeable symptoms, human hosts have a permanent relationship with this virus.
We anticipate that differences in viral virulence genes contribute to the differing symptoms and severity of HSV disease in humans. Are neuronal defenses activated during viral reactivation, or only during the initial round of infection?

The consequences of HSV latency for the neurons that harbor this pathogen are not well understood. Our laboratory aims to address this question and search for improved therapeutics using a combination of virology, neurobiology, next generation sequencing technologies, and bioinformatics. We address the neurobiology of infection using a combination of neuronal cultures, in vivo models of infection, and high-throughput measurements of the host response.

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