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1. Coronaviruses are a family of viruses that includes viruses that may cause a range of illnesses in humans, from common cold-type respiratory infections to SARS. Viruses of this family also cause a number of animal diseases.

2. What’s it called again?
Currently being referred to as nCoV or nCoV-2012, this virus has also been called Human Coronavirus-Erasmus Medical Center (hCoV-EMC), or Middle East respiratory syndrome coronavirus (MERS-CoV), and even “Saudi SARS” (it’s not – SARS is a related but different Coronavirus).

3. The first known case of nCoV infection was in a Saudi Arabian man who died in early 2012. This particular strain of coronavirus had not been previously identified in humans. The second confirmed case appeared in early September 2012, involving a 49-year old man in Doha, Qatar who had traveled to Saudi Arabia around the same time that the first case was identified. Currently, at least 40 cases have been confirmed, and 20 of those affected have died. The virus has also been found in Tunisia.

4. Where did it come from?
Bats. (It’s [nearly] always bats.) Bat coronaviruses carried by the genus Pipistrellus that differ from nCoV by as little as 1.8%. The existence of over 50 species of Pipistrellus bats in the Arabian Peninsula suggests that they may be the animal reservoir.

5. Symptoms of nCoV infection include renal failure and severe acute pneumonia, which often result in a fatal outcome. In humans, the virus has a strong tropism for nonciliated bronchial epithelial cells because it uses dipeptidyl peptidase 4 (DPP4, also known as CD26) as a receptor.

6. nCoV can penetrate the bronchial epithelium and evade the innate immune system, signs that it is well-equipped for infecting human cells. This suggests that although nCoV may have jumped from animals to humans very recently, it is as well adapted to infecting the human respiratory tract as other, more familiar human coronaviruses, including the SARS virus and the common cold Coronavirus HCoV-229E.

7. The virus is susceptible to treatment with interferons, immune proteins that have been used successfully to treat other viral diseases, offering a possible method of treatment in the event of a large-scale outbreak.

8. How is it transmitted?
Almost certainly like other respiratory viruses, via aerosol droplets from coughs and sneezes, but possibly also by unwashed hands contaminated with respiratory secretions.

9. Is there a vaccine?
Not yet. It is possible to make vaccines agains Coronaviruses and several SARS vaccines were developed but never put into use because the SARS outbreak died away. It should be possible to make a nCoV vaccine if we need one.

10. Is there any travel advice?
At the moment the World Health Organization says there is no reason to impose any travel restrictions. Travel advice will be kept under review if additional cases occur or when the patterns of transmission become clearer.

11. Are we all going to die?
Probably not. Most of the people who have been infected so far have been older men, often with other medical conditions. The outbreak of Severe Acute Respiratory Syndrome (SARS) in 2003 infected over 8000 people and killed nearly 800 before burning itself out. But SARS didn’t kill us all and it’s unlikely that nCoV will either.

Other things you should know:

• 10 things you should know about H1N1 (swineflu)
• 10 things you should know about E. coli
• 10 things you didn’t know about Schmallenberg virus
• 10 things about Foot and Mouth Disease

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Tamiflu drug bill “shocking waste of taxpayers’ money”?

Uh, yeah, you wouldn’t be saying that if the swine flu pandemic hadn’t turned out to be as mild as it was. 

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The prospects and challenges of universal vaccines for influenza

Vaccination is the most effective way to reduce the impact of epidemic as well as pandemic influenza. However, the licensed inactivated influenza vaccine induces strain-specific immunity and must be updated annually. When novel viruses appear, matched vaccines are not likely to be available in time for the first wave of a pandemic. Yet, the enormous diversity of influenza A viruses in nature makes it impossible to predict which subtype or strain will cause the next pandemic. Several recent scientific advances have generated renewed enthusiasm and hope for universal vaccines that will induce broad protection from a range of influenza viruses.

Trends Microbiol. 2013 May 16. pii: S0966-842X(13)00074-7. doi: 10.1016/j.tim.2013.04.003

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Irish potato famine mystery solved after 168 years

Scientists believe they have finally identified the pathogen that caused the Irish potato famine. BBC News reports a research team led by The Sainsbury Laboratory in Norwich, England, used dried leaf cuttings — some of which are nearly 170 years old — to reconstruct the spread of the HERB-1 strain of Phytophthora infestans, a fungal disease that came to Ireland via Mexico in 1845. The disease destroyed potato crops and caused the deaths of a million people.

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Schmallenberg vaccine available to UK farmers this summer

Vaccine will prevent a disease that causes severe birth defects and miscarriages in livestock.

All about Schmallenberg virus: http://goo.gl/fuPyT

A new vaccine is being made available to prevent a disease which causes severe birth defects and miscarriages in livestock. Schmallenberg virus, which emerged in the Netherlands and Germany in 2011 and has been seen in cattle and sheep in the UK since early 2012, has been identified on more than 1,700 farms across the country. Adult animals infected during pregnancies in the autumn by virus-carrying midges, thought to have blown across the Channel, have given birth to deformed or stillborn lambs and calves.  UK farmers are the first in the European Union to have access to a vaccine against Schmallenberg, which will be available for vaccinating livestock this summer before most animals become pregnant again.

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Friendly Viruses Protect Us Against Bacteria

One of our most important lines of defense against bacterial invaders is mucus. The slimy substance coats the inside of the mouth, nose, eyelids, and digestive tract, to name just a few places, creating a barrier to the outside world. Mucus is also home to phages, viruses that infect and kill bacteria. They can be found wherever bacteria reside, but Jeremy Barr and his colleagues noticed that there were even more phages in mucus than in mucus-free areas just millimeters away. The saliva surrounding human gums, for example, had about five phages to every bacterial cell, while the ratio at the mucosal surface of the gum itself was closer to 40 to 1. The researchers found that the phages are studded with antibody-like molecules that grab onto the sugar chains in mucins. This keeps the phages in the mucus, where they have access to bacteria, and suggests that the viruses and the mucus-producing tissue have adapted to be compatible with each other. 

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Group C adenoviruses also encode two small RNAs, called virus-associated (VA) RNAI and VA RNAII. They are non-coding RNAs and transcribed by RNA polymerase III. Both VA RNAs are about 160 nucleotides long and GC rich. Expression of the VA RNAs begins during the early phase of infection and increases rapidly to a high level during the late phase. Inactivation of VA RNAI results in a 10–20 fold decrease in virus production, whereas deletion of VA RNAII alone has little impact on virus replication. The functional significance of VA RNAI is well documented whereas little is known about the function of VA RNAII. The primary function of VA RNAI appears to be to block the activity of RNA-dependent protein kinase (PKA), a double-strained RNA activated inhibitor of translation. VA RNAI also stabilizes ribosome-associated viral mRNAs resulting in enhanced levels of viral protein synthesis. In addition, VA RNAI binds efficiently to Exportin 5, interfering with the nuclear export of the cellular RNAi and miRNA precursors and Dicer processing. Finally, large amounts of VA RNA-derived small RNAs associate with RNA-induced silencing (RISC) complexes.

During the last decade, increasing numbers of small RNAs have been identified and characterized and it has become evident that the small RNAs are critical regulators of gene function (Bartel, 2004, Seto et al., 2007 and Zaratiegui et al., 2007). There are three main categories: short interfering RNAs (siRNAs which are ∼21 nt in length), microRNAs (miRNAs, ∼22 nt in length) and PIWI-interacting RNAs (piRNAs, ∼24–32 nt in length). Deep sequencing technologies combined with bioinformatic strategies have revolutionized the identification of rare small RNAs. This study examines the expression of adenovirus-encoded small RNAs at different times after infection using deep sequencing. Adenovirus-encoded small RNAs may thus constitute a front-line defense and be crucial for the survival of the virus.

Identification of adenovirus-encoded small RNAs by deep RNA sequencing. Virology. 06 May 2013. pii: S0042-6822(13)00200-6. doi: 10.1016/j.virol.2013.04.006
Using deep RNA sequencing, we have studied the expression of adenovirus-encoded small RNAs at different times after infection. Nineteen small RNAs which comprised more than 1% of the total pool of small RNAs at least one time point were identified. These small RNAs were between 25 and 35 nucleotides long and mapped in the region of the VA RNAI and RNAII genes. However, the overlap was incomplete and some contained a few extra nucleotides at the 3′ end. This finding together with the observation that some of the small RNAs were detected before VA RNA expression had started might indicate that they are derived from other precursors than VA RNAI and II. Interestingly, the small RNAs displayed different expression profiles during the course of the infection suggesting that they have different functions. An effort was made to identify their mRNA targets by using computer prediction and deep cDNA sequencing. The most significant targets for the earliest small RNAs were genes involved in signaling pathways.

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Hospital superbug not monitored by government

Doctors are unsure how many patients have been killed by carbapenemase-producing enterobacteriaceae.

Hospitals in England are not required to officially report infections of a “superbug” capable of resisting our most powerful antibiotics. Cases of “carbapenemase-producing enterobacteriaceae” (CPE) have shown a sharp rise. Public Health England said a lack of mandatory reporting made assessing the true extent of the problem difficult.

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The Secret Life of Virus Glycoproteins

Viruses have developed remarkable mechanisms to inhibit the adaptive and innate immune systems of their hosts. Clearly, viral entry glycoproteins play critical roles in these activities. However, many of these roles and biological pathways are poorly defined. With new infectious diseases emerging and classical viral diseases reemerging, closer examination of viral entry glycoproteins as targets for preventative or therapeutic strategies is warranted.

http://www.microbiologybytes.com/blog/2013/05/20/the-secret-life-of-virus-glycoproteins/ 

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