Coronavirus Infection and Prostaglandins.

Author.

Hayk S. Arakelyan. Full Professor in Medicine,

Doctor of Medical Sciences, Ph.D , Grand Ph.D .

Senior Expert of Interactive Clinical Pharmacology , Drug Safety,

Treatment Tactics, General Medicine and Clinical Research.

“It is health that is real wealth and not pieces of gold and silver”. 

“Mahatma Gandhi”

Introduction.

During several months of 2003, a newly identified illness termed severe acute
respiratory syndrome (SARS) spread rapidly through the world. A new coronavirus
(SARS-CoV) was identified as the SARS pathogen , which triggered severe
pneumonia and acute, often lethal, lung failure8. Moreover, among infected
individuals influenza such as the Spanish flu9,10 and the emergence of new
respiratory disease viruses  have caused high lethality resulting from acute lung
failure.

Coronavirus Infection and Prostaglandins.

Several prostaglandins are continuously produced in every cell. They activate

protein kinases by regulating cyclic nucleotide synthesis. Modifications of the
phosphorylation of virus polypeptides and alterations in the microtubular system of
host cells can result in the reactivation of latent viruses. Prostaglandins have a very
important role in directing cell cycle. Abnormal tyrosine kinase activities during
viral cell transformation are responsible for the malignant changes and
consequently severe alterations are observed in the endogenous prostaglandin
production. External modification of this cascade can revert malignant signs to
normal. Furthermore, virus infection or cell transformation could be
promoted by the immunosuppressive effects of overproduced prostaglandins.
They damage interferon release and co-operation between the different cell
types of the immune system. Enzyme inhibitors of the prostaglandin cascade or
prostaglandin analogues may exert influence on all of these phenomenon,
providing future therapeutic agents. PGA1 was found to be effective in several cell
and virus models, suggesting a broad spectrum of antiviral actions.

 Infection of these cells with Sendai virus did not alter rates of PGE1 synthesis,
while it stimulated interferon production. PGAs, that we have previously shown to
be potent inhibitors of Sendai virus replication in this system, at the same dose (4
μg/ml), also strongly inhibited the replication of this virus in HEp-2 cells and in
VERO cells, a monkey kidney cell line that does not produce interferon. PGA1 was
found to be effective in several cell and virus models, suggesting a broad spectrum
of antiviral actions. Finally, we confirmed the observation that PGA1-treatment
prevents the establishment of a “carrier state” by Sendai virus, and PGA1-
cured cells did not show any sign of persistent infection for periods as long as
110 days after Sendai function. Inflammatory responses to viral infections must
be optimized to clear the pathogen without tissue damage. Inflammasomes
comprise an important component of the innate immune response. Prostaglandin
D2 (PGD2), an eicosanoid with both pro- and anti-inflammatory properties, is the
most abundantly expressed prostaglandin. PGD2 signaling through the D-
prostanoid receptor 1 (DP1) receptor is necessary for optimal
microglia/macrophage activation and IFN expression after infection with a
neurotropic coronavirus. Genome-wide expression analyses indicated that
PGD2/DP1 signaling is required for up-regulation of a putative inflammasome
inhibitor.

If you have any questions concerning “Coronavirus Infection and

Prostaglandins”, interactive clinical pharmacology , or any other questions,

please inform  me . 

      Prof. Hayk S. Arakelyan