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A Flu Virus That Killed Millions In 1918 Has Now Been Recreated


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Spanish flu

Scientists have recreated a nearly exact replicate of the deadly flu virus that killed an estimated 50 million in the 1918 Spanish flu pandemic.

But don’t worry, they say it’s totally safe.

Researchers at the University of Wisconsin-Madison reverse engineered an influenza virus from a similar one found in birds, combining several strains to create one that is nearly identical to the one that caused the 1918 outbreak. They then mutated the genes to make it airborne, and to study how it spreads between animals.

“Our research indicates the risks inherent in circulating avian influenza viruses,” Yoshihiro Kawaoka, the scientist who led the research team, told VICE News. “Continued surveillance of avian influenza viruses — and not only viruses that we know pose risks for humans, such as H5N1 and H7N9 influenza viruses, and attention to pandemic preparedness measures is important.”

According to the statement summarizing the project published this week, the “analyses revealed the global prevalence of avian influenza virus genes whose proteins differ only a few amino acids from the 1918 pandemic influenza virus, suggesting that 1918-like pandemic viruses may emerge in the future.”

In other words, a common avian flu virus that has been circulating in wild ducks is pretty much the exact same one that infected humans a century ago. And now is in a lab.

The research was funded by the National Institute of Health as a way to find out more about similar virus’ and their transmissibility from animals to humans. It was done in a lab that complied with full safety and security regulations, said Carole Heilman, director of the Division of Microbiology and Infectious Diseases, at National Institute of Allergy and Infectious Diseases (NIAD), a division of NIH.

“It was an question of risk versus benefit,” Heilman told VICE News. “We determined that the risk benefit ratio was adequate if we had this type of safety regulations.”

But many scientists disagree and have condemned research that recreates virus’ such this, stating that if released accidentally, a virus could spread to humans and cause a pandemic. Marc Lipsitch, an epidemiologist at Harvard, has criticized research such as Kawaoka’s as unnecessarily risky.

“There is a quantifiable possibility that these novel pathogens could be accidentally or deliberately released. Exacerbating the immunological vulnerability of human populations to PPPs is the potential for rapid global dissemination via ever-increasing human mobility,” Lipsitch said in a paper about experiments with transmissible virus’. “The dangers are not just hypothetical.”

Lipsitch points out that many of the H1N1 flu outbreaks that have occurred between 1977 and 2009 were a result of a lab accident.

Kawaoka disagrees, saying, “We maintain that it is better to know as much as possible about the risk posed by these viruses so we may be able to identify the risk when viruses with pandemic potential emerge, and have effective countermeasures on-hand or ready for development.”

This article originally appeared at VICE News. Check them out on YouTube, Facebook, and Instagram. Copyright 2014. Follow VICE News on Twitter.

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Clinical Syndromes, Laboratory Diagnosis and Treatment of Orthomyxoviruses

February 12, 2012 3 comments

Clinical Syndromes

Depending on the degree of immunity to the infecting strain of virus and other factors, infection may range from asymptomatic to severe. Patients with underlying cardiorespiratory disease, people with immune deficiency (even that associated with pregnancy), the elderly, and smokers are more prone to have a severe case.

After an incubation period of 1 to 4 days, the “flu syndrome” begins with a brief prodrome of malaise and headache lasting a few hours. The prodrome is followed by the abrupt onset of fever, chills, severe myalgias, loss of appetite, weakness and fatigue, sore throat, and usually a nonproductive cough. The fever persists for 3 to 8 days, and unless a complication occurs, recovery is complete within 7 to 10 days. Influenza in young children (under 3 years) resembles other severe respiratory tract infections, causing bronchiolitis, croup, otitis media, vomiting, and abdominal pain, accompanied rarely by febrile convulsions (Table 1). Complications of influenza include bacterial pneumonia, myositis, and Reye syndrome. The central nervous system can also be involved. Influenza B disease is similar to influenza A disease.

Influenza may directly cause pneumonia, but it more commonly promotes a secondary bacterial superinfection that leads to bronchitis or pneumonia. The tissue damage caused by progressive influenza virus infection of alveoli can be extensive, leading to hypoxia and bilateral pneumonia. Secondary bacterial infection usually involves Streptococcus pneumoniae, Haemophilus influenzae, or Staphylococcus aureus. In these infections, sputum usually is produced and becomes purulent.

Although the infection generally is limited to the lung, some strains of influenza can spread to other sites in certain people. For example, myositis (inflammation of muscle) may occur in children. Encephalopathy, although rare, may accompany an acute influenza illness and can be fatal. Postinfluenza encephalitis occurs 2 to 3 weeks after recovery from influenza. It is associated with evidence of inflammation but is rarely fatal.

Reye syndrome is an acute encephalitis that affects children and occurs after a variety of acute febrile viral infections, including varicella and influenza B and A diseases. Children given salicylates (aspirin) are at increased risk for this syndrome. In addition to encephalopathy, hepatic dysfunction is present. The mortality rate may be as high as 40%.

Laboratory Diagnosis

The diagnosis of influenza is usually based on the characteristic symptoms, the season, and the presence of the virus in the community. Laboratory methods that distinguish influenza from other respiratory viruses and identify its type and strain confirm the diagnosis (Table 2).

Influenza viruses are obtained from respiratory secretions. The virus is generally isolated in primary monkey kidney cell cultures or the Madin-Darby canine kidney cell line. Nonspecific cytopathologic effects are often difficult to distinguish but may be noted within as few as 2 days (average, 4 days). Before the cytopathologic effects develop, the addition of guinea pig erythrocytes may reveal hemadsorption (the adherence of these erythrocytes to HA-expressing infected cells). The addition of influenza virus-containing media to erythrocytes promotes the formation of a gel-like aggregate due to hemagglutination. Hemagglutination and hemadsorption are not specific to influenza viruses, however; parainfluenza and other viruses also exhibit these properties.

More rapid techniques detect and identify the influenza genome or antigens of the virus. Rapid antigen assays (less than 30 min) can detect and distinguish influenza A and B. Reverse transcriptase polymerase chain reaction (RT-PCR) using generic influenza primers can be used to detect and distinguish influenza A and B, and more specific primers can be used to distinguish the different strains, such as H5N1. Enzyme immunoassay or immunofluorescence can be used to detect viral antigen in exfoliated cells, respiratory secretions, or cell culture and are more sensitive assays. Immunofluorescence or inhibition of hemadsorption or hemagglutination (hemagglutination inhibition [HI]) with specific antibody can also detect and distinguish different influenza strains. Laboratory studies are primarily used for epidemiologic purposes.

To read more click on this link to the full article: Clinical Syndromes, Laboratory Diagnosis and Treatment of Orthomyxoviruses

Debating research into mutant H5N1 flu virus

February 8, 2012 1 comment

On 2 February, scientists and public health officials squared off in a panel discussion at the New York Academy of Sciences. At stake, the fate of two papers which describe a mutant strain of the avian influenza virus H5N1. The virus is capable of mammal-to-mammal transmission, which has raised concern that it might be transferable to humans. Several panelists sat down with Nature News to discuss their positions prior to the panel discussion.

For more on the NYAS debate, visit Nature’s blog:

http://blogs.nature.com/news/2012/02/emotion-runs-high-at-h5n1-debate.html

and see web special about the ongoing controversy over H5N1:

http://www.nature.com/news/specials/mutantflu/index.html

Or see NYAS.org where the NYAS has posted two hours of video from the H5N1 event. Now everyone can see exactly what Mike Osterholm said to Peter Palese. Highly unprofessional, in my opinion, and not conducive with a good scientific discourse. Laurie Garrett was not much better.

“Dual Use Research: H5N1 Influenza Virus and Beyond” Panel Sparks Lively Debate | The New York Acade

Pathogenesis and Epidemiology of Orthomyxoviruses

February 3, 2012 Leave a comment

Pathogenesis and Immunity

Influenza initially establishes a local upper respiratory tract infection. To do so, the virus first targets and kills mucus-secreting, ciliated, and other epithelial cells, causing the loss of this primary defense system. NA facilitates the development of the infection by cleaving sialic acid residues of the mucus, thereby providing access to tissue. Preferential release of the virus at the apical surface of epithelial cells and into the lung promotes cell-to-cell spread and transmission to other hosts. If the virus spreads to the lower respiratory tract, the infection can cause severe desquamation (shedding) of bronchial or alveolar epithelium down to a single-cell basal layer or to the basement membrane.

In addition to compromising the natural defenses of the respiratory tract, influenza infection promotes bacterial adhesion to the epithelial cells. Pneumonia may result from a viral pathogenesis or from a secondary bacterial infection. Influenza may also cause a transient or low-level viremia but rarely involves tissues other than the lung.

Histologically, influenza infection leads to an inflammatory cell response of the mucosal membrane, which consists primarily of monocytes and lymphocytes and few neutrophils. Submucosal edema is present. Lung tissue may reveal hyaline membrane disease, alveolar emphysema, and necrosis of the alveolar walls

Interferon and cytokine responses peak at almost the same time as virus in nasal washes and are concomitant with the febrile phase of disease. T-cell responses are important for effecting recovery and immunopathogenesis. However, influenza infection depresses macrophage and T-cell function, hindering immune resolution. Interestingly, recovery often precedes detection of antibody in serum or secretions.

Protection against reinfection is primarily associated with the development of antibodies to HA, but antibodies to NA are also protective. The antibody response is specific for each strain of influenza, but the cell-mediated immune response is more general and is capable of reacting to influenza strains of the same type (influenza A or B virus). Antigenic targets for T-cell responses include peptides from HA but also from the nucleocapsid proteins (NP, PB2) and M1 protein. The NP, PB2, and M1 proteins differ considerably for influenza A and B but not between strains of these viruses; hence T-cell memory may provide future protection against infection by different strains of either influenza A or B.

The symptoms and time course of the disease are determined by interferon and T-cell responses and the extent of epithelial tissue loss. Influenza is normally a self-limited disease that rarely involves organs other than the lung.Many of the classic “flu” symptoms (e.g., fever, malaise, headache, and myalgia) are associated with interferon induction. Repair of the compromised tissue is initiated within 3 to 5 days of the start of symptoms but may take as long as a month or more, especially for elderly people.

To read more click on this link to the full article: Pathogenesis and Epidemiology of Orthomyxoviruses

Structure and Replication of Orthomyxoviruses

January 31, 2012 1 comment

Introduction

Influenza A, B, and C viruses are the only members of the Orthomyxoviridae family, and only influenza A and B viruses cause significant human disease. The orthomyxoviruses are enveloped and have a segmented negative-sense RNA genome. The segmented genome of these viruses facilitates the development of new strains through the mutation and reassortment of the gene segments among different human and animal (influenza A) strains of virus. This genetic instability is responsible for the annual epidemics (mutation: drift) and periodic pandemics (reassortment: shift) of influenza infection worldwide.

Influenza is one of the most prevalent and significant viral infections. There are even descriptions of influenza epidemics (local dissemination) that occurred in ancient times. Probably the most famous influenza pandemic (worldwide) is the Spanish influenza that swept the world in 1918 to 1919, killing 20 to 40 million people. In fact, more people died of influenza during that time than in the battles of World War I. Pandemics caused by novel influenza viruses occurred in 1918, 1947, 1957, 1968, and 1977, but fortunately none have occurred since. New virus strains have been detected since the last pandemic, including an outbreak of avian influenza first noted in Hong Kong in 1997, which has caused some human disease and fatalities. Fortunately, prophylaxis in the form of vaccines and antiviral drugs is now available for people at risk for serious outcomes.

To read more click on this link to the full article: Structure and Replication of Orthomyxoviruses.