$GWPC & Ebola! $GWPC getting hot! $GWPC ebola viru
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Posted On: 10/23/2014 12:06:45 PM
$GWPC & Ebola! $GWPC getting hot! $GWPC ebola virus is an aggressive pathogen that causes a highly lethal hemorrhagic fever syndrome in humans and nonhuman primates.
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First recognized near the Ebola River valley during an outbreak in Zaire in 1976 (6, 20), outbreaks have occurred in Africa in the ensuing 27 years, with mortality rates ranging from 50 to 90% (26, 28). Outbreaks have been identified yearly for the past 3 years in central Africa, the most recent of which continues in the Republic of the Congo, with more than 125 fatalities to date according to the World Health Organization (http://www.who.int/csr/don/2003_05_07/en/, accessed 7 May 2003). The natural host for Ebola virus is unknown, so it has not been possible to implement programs to control or eliminate viral reservoirs of transmission to human populations. The rapid progression of Ebola virus infection has further complicated the control of this disease, affording little opportunity to develop acquired immunity. There is currently no antiviral therapy or vaccine that is effective against Ebola virus infection in humans.
Although its clinical course is well known, the specific mechanisms underlying the pathogenicity of Ebola virus have not been clearly delineated. This is due, in part, to the difficulty in obtaining samples and studying the disease in the relatively remote areas in which the outbreaks occur. In addition, a high degree of biohazard containment is required for laboratory studies and clinical analysis. Isolation of the viral cDNAs and the development of expression systems have allowed the study of Ebola virus gene products under less restrictive conditions and facilitated an understanding of the mechanisms underlying virally induced cell damage.
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EBOLA VIRUS DISEASE PROGRESSION
Typically, Ebola virus infection runs its course within 14 to 21 days. Infection initially presents with nonspecific flu-like symptoms such as fever, myalgia, and malaise. As the infection progresses, patients exhibit severe bleeding and coagulation abnormalities, including gastrointestinal bleeding, rash, and a range of hematological irregularities, such as lymphopenia and neutrophilia. Cytokines are released when reticuloendothelial cells encounter virus, which can contribute to exaggerated inflammatory responses that are not protective. Damage to the liver, combined with massive viremia, leads to disseminated intravascular coagulopathy. The virus eventually infects microvascular endothelial cells and compromises vascular integrity. The terminal stages of Ebola virus infection usually include diffuse bleeding, and hypotensive shock accounts for many Ebola virus fatalities (for reviews, see references 9 and 28).
http://www.otcmarkets.com/stock/GWPC/news
First recognized near the Ebola River valley during an outbreak in Zaire in 1976 (6, 20), outbreaks have occurred in Africa in the ensuing 27 years, with mortality rates ranging from 50 to 90% (26, 28). Outbreaks have been identified yearly for the past 3 years in central Africa, the most recent of which continues in the Republic of the Congo, with more than 125 fatalities to date according to the World Health Organization (http://www.who.int/csr/don/2003_05_07/en/, accessed 7 May 2003). The natural host for Ebola virus is unknown, so it has not been possible to implement programs to control or eliminate viral reservoirs of transmission to human populations. The rapid progression of Ebola virus infection has further complicated the control of this disease, affording little opportunity to develop acquired immunity. There is currently no antiviral therapy or vaccine that is effective against Ebola virus infection in humans.
Although its clinical course is well known, the specific mechanisms underlying the pathogenicity of Ebola virus have not been clearly delineated. This is due, in part, to the difficulty in obtaining samples and studying the disease in the relatively remote areas in which the outbreaks occur. In addition, a high degree of biohazard containment is required for laboratory studies and clinical analysis. Isolation of the viral cDNAs and the development of expression systems have allowed the study of Ebola virus gene products under less restrictive conditions and facilitated an understanding of the mechanisms underlying virally induced cell damage.
Next Section
EBOLA VIRUS DISEASE PROGRESSION
Typically, Ebola virus infection runs its course within 14 to 21 days. Infection initially presents with nonspecific flu-like symptoms such as fever, myalgia, and malaise. As the infection progresses, patients exhibit severe bleeding and coagulation abnormalities, including gastrointestinal bleeding, rash, and a range of hematological irregularities, such as lymphopenia and neutrophilia. Cytokines are released when reticuloendothelial cells encounter virus, which can contribute to exaggerated inflammatory responses that are not protective. Damage to the liver, combined with massive viremia, leads to disseminated intravascular coagulopathy. The virus eventually infects microvascular endothelial cells and compromises vascular integrity. The terminal stages of Ebola virus infection usually include diffuse bleeding, and hypotensive shock accounts for many Ebola virus fatalities (for reviews, see references 9 and 28).
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