Re: Herpesviruses secrete phony IL-10; might cause autoimmune risk
Kofi
Hasenkam" <jo...@goawayplease.com> wrote:
> Kofi,
>
> You might want to look up cannabinoids and Herpes Simplex, I think there
> was
> a study released a few months ago suggesting some cannabinoids can
> inhibit
> herbes replication. Interesting given the success of cannabinoids in
> Multiple Sclerosis.
Nice find. Have you got anything more recent than what I dug up - like
an in vivo study?
This fits in with my theory that low-dose naltrexone stimulates
cannabinoid signaling via upregulating the mu opioid receptor.
BMC Med. 2004 Sep 15;2:34.
Delta-9 tetrahydrocannabinol (THC) inhibits lytic replication of gamma
oncogenic herpesviruses in vitro.
Medveczky MM, Sherwood TA, Klein TW, Friedman H, Medveczky PG.
Department of Medical Microbiology and Immunology, MDC Box 10,
University of South Florida, and the H. Lee Moffitt Cancer Center, 12901
Bruce B. Downs Blvd, Tampa, FL 33612-4799, USA.
BACKGROUND: The major psychoactive cannabinoid compound of marijuana,
delta-9 tetrahydrocannabinol (THC), has been shown to modulate immune
responses and lymphocyte function. After primary infection the viral DNA
genome of gamma herpesviruses persists in lymphoid cell nuclei in a
latent episomal circular form. In response to extracellular signals, the
latent virus can be activated, which leads to production of infectious
virus progeny. Therefore, we evaluated the potential effects of THC on
gamma herpesvirus replication. METHODS: Tissue cultures infected with
various gamma herpesviruses were cultured in the presence of increasing
concentrations of THC and the amount of viral DNA or infectious virus
yield was compared to those of control cultures. The effect of THC on
Kaposi's Sarcoma Associated Herpesvirus (KSHV) and Epstein-Barr virus
(EBV) replication was measured by the Gardella method and replication of
herpesvirus saimiri (HVS) of monkeys, murine gamma herpesvirus 68 (MHV
68), and herpes simplex type 1 (HSV-1) was measured by yield reduction
assays. Inhibition of the immediate early ORF 50 gene promoter activity
was measured by the dual luciferase method. RESULTS: Micromolar
concentrations of THC inhibit KSHV and EBV reactivation in virus
infected/immortalized B cells. THC also strongly inhibits lytic
replication of MHV 68 and HVS in vitro. Importantly, concentrations of
THC that inhibit virus replication of gamma herpesviruses have no effect
on cell growth or HSV-1 replication, indicating selectivity. THC was
shown to selectively inhibit the immediate early ORF 50 gene promoter of
KSHV and MHV 68. CONCLUSIONS: THC specifically targets viral and/or
cellular mechanisms required for replication and possibly shared by
these gamma herpesviruses, and the endocannabinoid system is possibly
involved in regulating gamma herpesvirus latency and lytic replication.
The immediate early gene ORF 50 promoter activity was specifically
inhibited by THC. These studies may also provide the foundation for the
development of antiviral strategies utilizing non-psychoactive
derivatives of THC.
Publication Types:
* Research Support, U.S. Gov't, P.H.S.
PMID: 15369590
Diabetes. 2001 Jul;50(7):1580-7.
Activation of acetyl-CoA carboxylase by a glutamate- and
magnesium-sensitive protein phosphatase in the islet beta-cell.
Kowluru A, Chen HQ, Modrick LM, Stefanelli C.
Department of Pharmaceutical Sciences, 610 Shapero Hall, Wayne State
University, Detroit, MI 48202, USA.
Acetyl-CoA carboxylase (ACC) catalyzes the formation of malonyl-CoA, a
precursor in the biosynthesis of long-chain fatty acids, which have been
implicated in physiological insulin secretion. The catalytic function of
ACC is regulated by phosphorylation (inactive)-dephosphorylation
(active). In this study we investigated whether similar regulatory
mechanisms exist for ACC in the pancreatic islet beta-cell. ACC was
quantitated in normal rat islets, human islets, and clonal beta-cells
(HIT-15 or INS-1) using a [(14)C]bicarbonate fixation assay. In the
beta-cell lysates, ACC was stimulated by magnesium in a
concentration-dependent manner. Of all the dicarboxylic acids tested,
only glutamate, albeit ineffective by itself, significantly potentiated
magnesium-activated ACC in a concentration-dependent manner. ACC
stimulation by glutamate and magnesium was maximally demonstrable in the
cytosolic fraction; it was markedly reduced by okadaic acid (OKA) in
concentrations (<50 nmol/l) that inhibited protein phosphatase 2A
(PP2A). Furthermore, pretreatment of the cytosolic fraction with
anti-PP2A serum attenuated the glutamate- and magnesium-mediated
activation of ACC, thereby suggesting that ACC may be regulated by an
OKA-sensitive PP2A-like enzyme. Streptavidin-agarose chromatography
studies have indicated that glutamate- and magnesium-mediated effects on
ACC are attributable to activation of ACC's dephosphorylation; this
suggests that the stimulatory effects of glutamate and magnesium on ACC
might involve activation of an OKA-sensitive PP2A-like enzyme that
dephosphorylates and activates ACC. In our study,
5-amino-imidazolecarboxamide (AICA) riboside, a stimulator of AMP
kinase, significantly inhibited glucose-mediated activation of ACC and
insulin secretion from isolated beta-cells. Together, our data provide
evidence for a unique regulatory mechanism for the activation of ACC in
the pancreatic beta-cell, leading to the generation of physiological
signals that may be relevant for physiological insulin secretion.
Publication Types:
* Research Support, Non-U.S. Gov't
* Research Support, U.S. Gov't, Non-P.H.S.
* Research Support, U.S. Gov't, P.H.S.
PMID: 11423479
John Hasenkam
"Kofi" <ko...@anon.un> wrote in message
news:kofi-5C5549.1...@news.west.earthlink.net...
> In article <1JSdnRCwQI0EPnXV...@westnet.com.au>, "John
> Hasenkam" <jo...@goawayplease.com> wrote:
>
>> Kofi,
>>
>> You might want to look up cannabinoids and Herpes Simplex, I think there
>> was
>> a study released a few months ago suggesting some cannabinoids can
>> inhibit
>> herbes replication. Interesting given the success of cannabinoids in
>> Multiple Sclerosis.
>
> Nice find. Have you got anything more recent than what I dug up - like
> an in vivo study?
>
> This fits in with my theory that low-dose naltrexone stimulates
> cannabinoid signaling via upregulating the mu opioid receptor.
>
>
This one address u opoid functions of cannabinoids.
http://molpharm.aspetjournals.org/cgi/reprint/69/4/1486.pdf
But can't find the original reference. In any event you've got the picture.
You might want to think about some heepseed, it is rich in cannabidiol.
You clearly are doing a great deal of research to address your problems.
Been there, done that. Had vision problems that left me unable to work for
many years. Saw doctors who all just said "get used to it". Bastards. Only
last year did I find the problem and within 2 months could start working
again because the cure was dead simple. Bloody doctors can be so lazy, if
the problem isn't in the textbooks too many of them just give up or worse
suspect you are malingering. Pricks.
Send me full details of your problems to jhas...@gmail.com. I'll see what
I can find for you.
John.