Guest guest Posted May 13, 2005 Report Share Posted May 13, 2005 I know that previously I posted that Losartan kept the herpes simplex virus lock in the cells.. and posted the reference... SEE REF #1 And we all thought that was a good thing... Well know it looks like the BO meds are selevtive in how they handel INF alpga, beta and gamma.. and these drugs can cause a LATENT virus (depending on the type of virus) to come OUT of Latency and cause disease and (death in the immunocompromised). ....SEE REF 2 SEE REF for: Latency/Cytomeglovirus and INF gamma: http://mstp.wustl.edu/alumni/rachel_presti.html IT LOOKS TO ME LIKE IF YOU ARE TAKING HIGH DOSE ARBS or ACE (and experiencing what you think are viral infections) you may want to read these and make your own conclusions. Barb Ref #1 ........................ Life Sci. 1994;55(4):283-9. Effects of the angiotensin II receptor antagonist losartan on herpes simplex virus-type 2 infection of cultured vero and cardiac neonatal myocytes. Gardner PL, Mbuy GN, Knabb MT. Department of Biology, West Chester University, PA 19383. Previous studies indicate that captopril, an angiotensin II converting enzyme inhibitor, attenuates cardiomyopathy in a murine viral myocarditis model. Accordingly, we investigated the ability of captopril as well as angiotensin II (AII) and losartan, a nonpeptide AII receptor antagonist, to alter infection or replication of herpes simplex virus- type 2 (HSV-2) in cultured cardiac and vero cells. Neither captopril nor AII influenced the ability of HSV-2 to replicate in either cell type. Losartan, however, caused a dose dependent decrease in pfu ability on vero cells with an ED50 of 1.35 mM. In cultured myocytes, losartan (400 microM) reduced significantly %LDH released (54.9 +/- 7.5 vs 29.1 +/- 4.2 in infected controls) and % pfu released (40.9 +/- 8.4 vs 14.8 +/- 3.8 in infected controls) into the media. REF # 2 ......................................... J Virol. 2002 Sep;76(18):9060-8. The antiviral response to gamma interferon. Costa-Pereira AP, TM, Strobl B, Watling D, Briscoe J, Kerr IM. Cancer Research UK London Research Institute, London WC2A 3PX, United Kingdom. A role for alpha/beta interferon (IFN-alpha/beta) in the IFN-gamma antiviral response has long been suggested. Accordingly, possible roles for autocrine or double-stranded-RNA (dsRNA)-induced IFN- alpha/beta in the IFN-gamma response were investigated. Use was made of wild-type and a variety of mutant human fibrosarcoma cell lines, including mutant U5A cells, which lack a functional IFN-alpha/beta receptor and hence an IFN-alpha/beta response. IFN-gamma did not induce detectable levels of IFN-alpha/beta in any of the cell lines, nor was the IFN-gamma response per se dependent on autocrine IFN- alpha/beta. On the other hand, a number of responses to dsRNA [poly (I). poly©] and encephalomyocarditis virus were greatly enhanced by IFN-gamma pretreatment (priming) of wild-type cells or of mutant cells lacking an IFN-alpha/beta response; these include the primary induction of dsRNA-inducible mRNAs, including IFN-beta mRNA, and, to a lesser extent, the dsRNA-mediated activation of the p38 mitogen- activated protein (MAP) kinase(s). IFN-gamma priming of mRNA induction by dsRNA is dependent on JAK1 and shows biphasic kinetics, with an initial rapid (<30-min) response being followed by a more substantial effect on overnight incubation. The IFN-gamma-primed dsRNA responses appear to be subject to modulation through the p38, phosphatidylinositol 3-kinase, and ERK1/ERK2 MAP kinase pathways. It can be concluded that despite efficient priming of IFN-beta production, the IFN-alpha/beta pathways play no significant role in the primary IFN-gamma antiviral response in these cell-virus systems. The observed IFN-gamma priming of dsRNA responses, on the other hand, will likely play a significant role in combating virus infection in vivo. Pharmaceuticals The Virus That Took Down Tysabri Herper, 03.02.05, 6:00 AM ET http://www.forbes.com/business/healthcare/2005/03/02/cx_mh_0301jcvirus ..html Quote Link to comment Share on other sites More sharing options...
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