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HTLV-1's replication: Perhaps it can explain XMRV's low degree of mutations

Discussion in 'XMRV Research and Replication Studies' started by omerbasket, Jun 9, 2011.

  1. tonydewitt

    tonydewitt

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    Newark, NJ
    The FDA is close to approving Tofacitinib for the treatment of Rheumatoid Arthritis (RA), but more importantly, the drug has been shown to be effective again BOTH disorders caused by HTLV, ATL and HAM (see article below). Therefore HTLV sufferers can tell their doctors "I have have arthritis" and receive actual treatment for their suffering!

    A Role for Tofacitinib Within the Treatment of ATL and HAM/TSP:
    The chemistry technology section at NCGC has aided the Waldmann lab (NCI) in using a Jak3 inhibitor for the potential treatment of ATL and HAM/TSP. The retrovirus, human T cell lymphotrophic virus-1 (HTLV-I) is the etiologic agent of adult T cell leukemia (ATL) and the neurological disorder, HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP). The HTLV-I encoded protein tax constitutively activates IL-2, IL-9 and IL-15 autocrine/paracrine systems, that in turn, activate the Jak3/STAT5 pathway, suggesting a therapeutic strategy that involves targeting Jak3.
    natasa778 likes this.
  2. xrayspex

    xrayspex Senior Member

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    u.s.a.
    I thought about testing for JAK 2 when I found out i have high b12, because that can be related....is jak3 similar to jak2? jak 2 are myloproliferative (sp) disorders
  3. tonydewitt

    tonydewitt

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    Newark, NJ
    Apoptosis.jpg JAK's are Janus Kinase, and the attached diagram (assuming that I can attach it) shows how interleukin can be stimulated by JAK to provide survival of HTLV infected cells. Inhibitors of JAK should allow those HTLV infected cells to die, which should help greatly in people suffering from HTLV caused disorders like HAM (paralysis) and ATL (leukemia). Examples of JAK inhibitors are AG490 and Tofacitinib (which is near approval by the FDA).
  4. tonydewitt

    tonydewitt

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    Newark, NJ
    Regarding your question about different JAKs, JAKs 1, 2, and 3 exist, but surprisingly Tofacitinib did as good a job of inhibiting all three as did separate inhibitors per JAK.

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