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Israel Steiner

Publications and source records attributed to Israel Steiner.

22 records · Page 2Linked to original sources
PubMed2002

Family with inflammatory demyelinating polyneuropathy and the HNPP 17p12 deletion.

Hereditary neuropathy with liability to pressure palsies (HNPP), classically presenting as recurrent focal neuropathies precipitated by trauma or compression, is an autosomal dominant neuropathy due to a deletion at chromosomal locus 17p12. Inflammatory demyelinating polyneuropathy (IDP), a putative autoimmune disorder presenting in an acute (AIDP) or a chronic form (CIDP), has been rarely reported as familial. We present a father and two daughters of Jewish Kurdish origin who developed IDP within 10 years. The unusual familial history led us to reevaluate the diagnosis of IDP, and suggested an autosomal dominant pedigree. DNA analysis identified the deletion typical of HNPP on chromosome 17. Screening for the HNPP deletion in patients with atypical, recurrent, or familial IDP might be warranted.

Adult↗
PubMed2002

The latency-associated gene of herpes simplex virus type 1 (HSV-1) interferes with superinfection by HSV-1.

During herpes simplex virus type 1 (HSV-1) lifelong latency in human peripheral sensory ganglia (PSG), only the viral latency-associated transcript (LAT) gene is expressed. This raises the possibility that this gene is involved in establishment of latency of the virus, its maintenance, or reactivation. Here we present data that indicate yet another independent function of the LAT gene: interference with HSV-1 superinfection of latently infected neurons. Neuronal cells stably expressing the LATs are protected from infection with HSV-1, but not from infection by other RNA and DNA viruses, including HSV-2. These unexpected findings may explain the observation that human PSG are latently infected with just a single strain of HSV-1, despite repeated exposure during life to multiple viral strains. Thus, the LATs may protect the latent HSV-1 reservoir from cytopathic superinfections, and at the same time the host is protected at the viral entry site from HSV-1 insults that may eventually cause viral encephalitis.

Herpes Simplex↗