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"Dengue is the leading mosquito-borne viral illness infecting humans !"
Dengue is caused by infection with any of the four dengue virus serotypes. This review highlights the mechanisms underlying the clinical course of a dengue infection, which can range from mild febrile illness through to hemorrhagic fever and circulatory shock. It also outlines the epidemiology, pathogenesis, diagnosis and management of dengue infection.
Key phases of dengue infection
Dengue is a mosquito-borne disease caused by infection with dengue virus (DENV). Clinically, the disease can range from a mild febrile illness (previously called dengue fever) through to dengue with warning signs and severe dengue, which includes what were previously called dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS).
DENVs belong to the genus Flavivirus of the Flaviviridae family. The four serotypes are enveloped, spherical viral particles with a diameter of approximately 500 Å20. The genome of each serotype comprises approximately 11 kb of positive-sense, single-stranded RNA that encodes ten proteins. The three structural proteins encoded by the genome are the membrane (M) protein, envelope (E) protein and capsid (C) protein; the non-structural (NS) proteins are NS1, NS2A, NS2B, NS3, NS4A, NS4B and NS5.
"The viral receptor on human cells plays a critical role in disease progression !"
Viruses enter cells and initiate infection by binding to their cognate cell surface receptors. The expression and distribution of viral entry receptors therefore regulates their tropism, determining the tissues that are infected and thus disease pathogenesis. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the third human coronavirus known to co-opt the peptidase angiotensin-converting enzyme 2 (ACE2) for cell entry. The interaction between SARS-CoV-2 and ACE2 is critical to determining both tissue tropism and progression from early SARS-CoV-2 infection to severe coronavirus disease 2019 (COVID-19). Understanding the cellular basis of SARS-CoV-2 infection could reveal treatments that prevent the development of severe disease, and thus reduce mortality.
Key phases of disease progression
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) binds to angiotensin-converting enzyme 2 (ACE2). Initial infection of cells in the upper respiratory tract may be asymptomatic, but these patients can still transmit the virus. For those who develop symptoms, up to 90% will have pneumonitis, caused by infection of cells in the lower respiratory tract. Some of these patients will progress to severe disease, with disruption of the epithelial-endothelial barrier, and multi-organ involvement.
As with all coronaviruses, SARS-CoV-2 cell entry is dependent on its 180-kDa spike (S) protein, which mediates two essential events: binding to ACE2 by the amino-terminal region, and fusion of viral and cellular membranes through the carboxyl-terminal region. Infection of lung cells requires host proteolytic activation of spike at a polybasic furin cleavage site. To date, this cleavage site is found in all spike proteins from clinical SARS-CoV-2 isolates, as well as some other highly pathogenic viruses (e.g., avian influenza A), but it is absent from SARS-CoV and is likely to have been acquired by recombination between coronaviruses in bats. Cleavage by the furin protease therefore expands SARS-CoV-2 cell tropism and may have facilitated transmission from bats to humans. Membrane fusion also requires cleavage by additional proteases, particularly transmembrane protease serine 2 (TMPRSS2), a host cell surface protease that cleaves spike shortly after binding ACE2. SARS-CoV-2 tropism is therefore dependent on expression of cellular proteases, as well as ACE2.
This is how Covid-19 is spreading pandemic across the globe !
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Watching carefully the entire video presents a very interesting and important hidden information how rapidly the virus at first spreads in China, then subsequently to other countries, at the same time how some countries including China were able to control and maintain the rate of spread while others such as Italy not able to and USA making to top !
Nipah virus (NiV) is a member of the family Paramyxoviridae, genus Henipavirus. NiV was initially isolated and identified in 1999 during an outbreak of encephalitis and respiratory illness among pig farmers and people with close contact with pigs in Malaysia and Singapore. Its name originated from Sungai Nipah, a village in the Malaysian Peninsula where pig farmers became ill with encephalitis. Given the relatedness of NiV to Hendra virus, bat species were quickly singled out for investigation and flying foxes of the genus Pteropus were subsequently identified as the reservoir for NiV (Distribution Map).
In the 1999 outbreak, Nipah virus caused a relatively mild disease in pigs, but nearly 300 human cases with over 100 deaths were reported. In order to stop the outbreak, more than a million pigs were euthanized, causing tremendous trade loss for Malaysia. Since this outbreak, no subsequent cases (in neither swine nor human) have been reported in either Malaysia or Singapore.
Hepatitis C (HCV) is a viral infection that affects the liver and an estimated 3.2 million people in the USA are infected with HCV, and most do not feel ill or know that they are infected. Since 2010, acute cases of HCV have more than doubled, with new cases predominantly among young, white individuals with a history of injection drug use.
The current recommendations are that doctors screen patients at high-risk for contracting HCV, which include but are not limited to people born between 1945 and 1965, those diagnosed with HIV, children born to HCV-positive women and individuals who engage in injection drug use (PWID), among other select populations at high risk. This strategy is called "targeted" screening. "Routine" screening, as defined in the study, tests all individuals in a community with a high prevalence of HCV.
Video: One step Hepatitis C Virus Test Cassette, Raecho International
There are two ways to perform these screenings. Rapid testing is when results are given on the same day that the sample is drawn. Standard testing requires patients to return for a second appointment to get the results. Scientists at Boston Medical Center (Boston, MA, USA) and their colleagues evaluated the clinical benefits and cost-effectiveness of testing strategies among 15 to 30-year-olds at urban community health centers. They developed a decision analytic model to project quality-adjusted life years (QALYs), lifetime costs (2016 USDs) and incremental cost-effectiveness ratios (ICER) associated with nine strategies for one-time testing. The strategies differed in three ways: targeted versus routine testing; rapid finger stick versus standard venipuncture; and ordered by physician versus counselor/tester using standing orders.
Illustration of the Hepatitis C Virus
The team found that compared to targeted risk-based testing (current standard of care), routine testing increased lifetime medical cost by USD 80 and discounted QALYs by 0.0013 per person. Across all strategies rapid testing provided higher QALYs at a lower cost per QALY gained, and was always preferred. Counselor-initiated routine rapid testing was associated with an ICER of USD 71,000/QALY gained. Results were sensitive to offer and result receipt rates. Counselor-initiated routine rapid testing was cost-effective (ICER greater than USD 100,000/QALY) unless the prevalence of PWID was greater than 0.59%, HCV prevalence among PWID less than 16%, reinfection rate greater than 26 cases per 100 person-years, or reflex confirmatory testing followed all reactive venipuncture diagnostics.
Sabrina A. Assoumou, MD, MPH, an infectious disease physician and lead author of the study, said, “When standard testing was applied, patients were less likely to come back for that second appointment to get their results, which in turn meant more people weren't getting the treatment they so desperately needed. Our results indicate that we must initiate rapid testing strategies so that more people will know their status and get treatment more quickly.” The study was published on September 9, 2017, in the journal Clinical Infectious Diseases.
It is estimated that in the USA influenza -related deaths in recent years have ranged from 12,000 to 56,000. Factors like age, obesity, pregnancy and such chronic health conditions as asthma, chronic lung disease and heart disease are associated with an elevated risk of complications and death.
However, there are no proven genetic markers of influenza risk with an established mechanism of action. Interferon Induced Transmembrane Protein 3 (IFITM3) is an anti-viral protein that helps to block influenza infection of lung cells and to promote survival of the killer T cells that help clear the infection in the airways.
Image: A scanning electron micrograph of a CD8+ T cell engaging a virus.
(Photo courtesy of Dennis Kunkel).
A group of scientists collaborating with those at St. Jude Children's Research Hospital (Memphis, TN, USA) searched for other possible IFITM3 variants that correlated with gene expression, levels of the IFITM3 proteins and were common in influenza patients in the USA. The search led to an IFITM3 variant known as rs34481144. They checked 86 children and adults in Memphis with confirmed influenza infections and found two-thirds of patients with the most severe symptoms carried at least one copy of the newly identified high-risk IFITM3 variant. The high-risk variant was found in just 32% of patients with milder symptoms.
The team also found an association between the newly identified high-risk variant and severe and fatal influenza infections in 265 critically ill pediatric patients hospitalized in one of 31 intensive care units nationwide. The patients did not have health problems that put them at high risk for severe influenza. Of the 17 patients in this group who died from the infection, 14 carried at least one copy of the newly identified high-risk variant. Further study revealed how binding differed between the high-risk and protective variants. Those differences led to lower levels of the IFITM3 protein in individuals with two copies of the high-risk gene variant compared to other patients. The Memphis influenza patients also had fewer of the killer T cells in their upper airways. The study identifies a new regulator of IFITM3 expression that associates with CD8+ T cell levels in the airways and a spectrum of clinical outcomes.
Paul Thomas, PhD, an immunologist and corresponding author of the study, said, “A genetic marker of influenza risk could make a life-saving difference, particularly during severe influenza outbreaks, by helping prioritize high-risk patients for vaccination, drug therapy and other interventions. These results raise hopes that this newly identified IFITM3 variant might provide such a marker.” The study was published on July 17, 2017, in the journal Nature Medicine.
An estimated 230,000 Australians have chronic hepatitis C, and a quarter of cases are undiagnosed.
Hepatitis C inflames the liver and unlike the A and B viruses there is no vaccine available. Pathology is important for diagnosing the virus.
Many people with hepatitis C may not experience symptoms, but left untreated the disease can cause cirrhosis (scarring of the liver), which in a small number of cases can lead to liver cancer.
Here it is again, the cold and flu season when we all head indoors to share our sneezes and viruses. It’s time to get serious about preventing illness, and that means caring for our personal air filter: the nose.
Viruses are the worst seasonal offenders, and colds are the most common virus we pass around. But the influenza virus is so much worse than a cold. Most folks do not really understand the difference between these two illnesses, yet the difference can be deadly.
Influenza, commonly called “the flu,” is caused by the influenza virus. This is a specific respiratory virus quite different than the cold virus. The entire respiratory tract—including the nose, throat, and lungs—becomes infected. The illness is severe and can be life-threatening; children, the elderly, and those who have underlying medical conditions are at greatest risk for complications.
From helping humans live longer and hacking our performance, to repairing the body and understanding the brain, WIRED Health will hear from the innovators transforming this critical sector.
Ten million people around the world will die each year by 2050 if more is not done to tackle the growing threat of antimicrobial resistance, Jim O'Neill, commercial secretary to the treasury, has said.
Speaking at WIRED Health, O'Neill said the rise in resistance needs to be "embraced by policy makers around the world".
If it isn't then the number of people dying from antimicrobial resistance (AMR) will increase dramatically.
Some 2.3 million people around the world are infected with both HIV and the hepatitis C virus (HCV) at the same time. The two are often intertwined, with HCV being the top cause of death aside from AIDS for co-infected patients. While there are currently vaccines for both hepatitis A and hepatitis B, there is no vaccine for hepatitis C. Likewise, HIV/AIDS treatment has improved significantly in recent decades, but there is still no vaccine.
In a new study, researchers note that a combined HIV and hepatitis C vaccine may soon be on the horizon. The study, which was presented at The International Liver Congress in Barcelona, describes how a combined vaccine would involve two main steps: first, exposing the immune system to adenoviral vectors that contain fragments of both HCV and HIV viruses, which would trigger antigens; and afterwards, administering booster vaccinations in an MVA vector containing the same HCV and HIV virus fragments.
“Finding effective vaccinations against the world’s biggest killers is a huge and pressing problem,” said Laurent Castera, Secretary General of the European Association for the Study of the Liver, in a statement. “This study shows for the first time that it is possible to generate simultaneous immune response against diseases HCV and HIV, raising the possibility of a combined vaccination.”
HIV, or the human immunodeficiency virus, causes HIV infection and over time, acquired immunodeficiency syndrome (AIDS). HCV is also a viral infection that mostly targets the liver, resulting in symptoms of fever, dark urine, stomach pain, and eventually liver disease, cirrhosis (scarring of the liver), or liver failure.
