Infection with herpes simplex virus (HSV) not only causes cerebral inflammation in people, some also believe this pathogen is a risk factor for Alzheimer's disease (see Alzheimer Hypotheses). Recently, rumors that HSV1 may have been detected in some of the patients who developed encephalitis in a failed clinical trial of Ab vaccination have again raised the question of exactly what happens when this virus is awakened from its latent stage inside neurons (see comment to vaccine live chat).

Today at the annual meeting of the American Academy of Neurology in Denver, Colorado, Roberta DeBiasi of the University of Colorado Health Sciences Center is presenting a poster on apoptosis in patients with herpes simplex encephalitis (HSE). Previous work on apoptosis in herpes-infected neurons was done in animal models (see, for example, Watanabe et al., 2000) or in immune-deficient people with HIV infection, in whom it is difficult to separate the effects of the virus from (impaired) immune responses by the host.

DeBiasi et al. analyzed tissue specimens from ten patients with HSE with antibodies against HSV, against activated caspase 3 (a protease known to be involved in programmed cell death), against the T cell marker CD3, and with TUNEL staining, a general apoptosis marker. The scientists found apoptotic neurons and glia in areas of active viral infection in patients with acute HSE and acute cytomegalovirus infection, but not in patients with chronic HSV encephalitis, nor in specimens infected with other viruses, such as enterovirus. "Apoptosis appeared to result from direct viral injury to neuronal cells, rather than as a consequence of secondary inflammatory response," the authors write. HSE is treatable, for example with acyclovir, but is still frequently fatal.-Gabrielle Strobel.

Reference:
DeBiasi RL, Kleinschmidt-DeMasters BK, Richardson-Burns S, Tyler KL. Human Herpes Simplex Encephalitis is Associated with CNS Apoptosis. Abstract P04.003.

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  1. Evidence for a link between apoptotic markers and HSV encephalitis is
    clearly a major step towards unraveling the mechanism by which HSV causes
    neurons and other brain cells to die. I'm not sure how it was determined
    that the apoptotic cells were actually neurons. I also think we need to be
    cautious about presuming that bonafide markers of well-defined pathways in
    other cell types are reliable indicators of the same pathway occurring in a
    postmitotic neuron. This precaution needs to be taken in the field of cell
    cycle research in AD, as well. The value of detecting any such marker in
    brain offers a new paradigm and perhaps a wealth of tools for further
    delineating the mechanism of degeneration of postmitotic neurons. This
    new information would then certainly better the chances of designing new
    therapeutic agents.

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References

Other Citations

  1. see Alzheimer Hypotheses

External Citations

  1. Watanabe et al., 2000

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