Posts Tagged ‘Influenza’
Two TED Talks on Influenza Pandemics
Saturday, May 2nd, 2009Laurie Garrett: What can we learn from the 1918 flu?
Larry Brilliant: Help stop the next pandemic
Change of name – swineflu is now H1N1
Thursday, April 30th, 2009
Originally, this darn virus infected pigs, and it was reasonable to call it swine flu (even though it appears that some people don’t know that “swine” means “pig” :-)
But after it jumped from pigs to humans – the World Health Organization agrees that extensive human-to-human transmission is now happening – it’s no longer reasonable to go on calling it swine flu, and we have to find a new name.
So I’m following President Obama’s example, and from now on, I’ll be calling it H1N1. This virus has a longer scientific name (to distinguish it from other H1N1 viruses), but everyone’s going to know what you mean, so H1N1 is OK. (By the way, it is formally H1N1, not h1n1, but no-one at MicrobiologyBytes is going to worry about that).
So if you want to stay up to date with all the latest news about the H1N1 pandemic, follow MicroBytes on Twitter, where you’ll get the latest and most accurate H1N1 news.
Now where’s that bacon sandwich? :-)
New influenza vaccine research at the University of Leicester
Tuesday, April 28th, 2009
New research published yesterday (Monday April 27) from the University of Leicester and University Hospitals of Leicester NHS Trust warns of a six-month time lag before effective vaccines can be manufactured in the event of an influenza pandemic. By that time, the first wave of pandemic flu may be over before people are vaccinated, says Dr Iain Stephenson, Consultant in Infectious Diseases at the Leicester Royal Infirmary and a Clinical Senior Lecturer at the University of Leicester.
Pandemic preparedness plans show that vaccination is critical for controlling pandemics. Some authorities have invested in vaccine stockpiles, but these resources are small in comparison to global demand. The use of stockpiled vaccine is challenged by the need for two doses and secondary manufacturing constraints. MF59, a proprietary adjuvant, was licensed in seasonal influenza vaccines in 1997, and more than 30 million doses have been administered safely so far. These new findings suggest that consideration could be given to advance priming to induce memory responses that enable cross-reactive antibodies to be generated rapidly after infection with the pandemic virus or by a single low-dose vaccination when required at the onset of future pandemic.
Fast rise of broadly cross-reactive antibodies after boosting long-lived human memory B cells primed by an MF59 adjuvanted prepandemic vaccine. PNAS USA April 27, 2009
Proactive priming before the next pandemic could induce immune memory responses to novel influenza antigens. In an open-label study, we analyzed B cell memory and antibody responses of 54 adults who received 2 7.5-μg doses of MF59-adjuvanted A/Vietnam/1194/2004 clade 1 (H5N1) vaccine. Twenty-four subjects had been previously primed with MF59-adjuvanted or plain clade 0-like A/duck/Singapore/1997 (H5N3) vaccine during 1999–2001. The prevaccination frequency of circulating memory B cells reactive to A/Vietnam/1194/2004 was low in both primed and unprimed individuals. However, at day 21 after boosting, MF59-adjuvanted primed subjects displayed a higher frequency of H5N1-specific memory B cells than plain-primed or unprimed subjects. The immune memory was rapidly mobilized by a single vaccine administration and resulted in high titers of neutralizing antibodies to antigenically diverse clade 0, 1, and 2 H5N1 viruses already at day 7. In general, postvaccination antibody titers were significantly higher in primed subjects than in unprimed subjects. Subjects primed with MF59-adjuvanted vaccine responded significantly better than those primed with plain vaccine, most notably in early induction and duration of cross-reacting antibody responses. After 6 months, high titers of cross-reactive antibody remained detectable among MF59-primed subjects. We conclude that distant priming with clade 0-like H5N3 induces a pool of cross-reactive memory B cells that can be boosted rapidly years afterward by a mismatched MF59-adjuvanted vaccine to generate high titers of cross-reactive neutralizing antibodies rapidly. These results suggest that pre-pandemic vaccination strategies should be considered.
Related:
- 10 things you should know about H1N1 (swineflu)
- 10 more things you should know about H1N1 (swineflu)
10 things you should know about H1N1 (swineflu)
Saturday, April 25th, 2009Latest News (unfiltered) | Latest news (filtered) (via Twitter)
1. What is swine flu?
Swine flu is a type of influenza virus. Influenza viruses are named after the proteins on the outside which are recognized by the body, H and N. There are dozens of combinations of these two proteins, each one giving a different type of influenza virus. Swine flu virus is H1N1 influenza. The original swine flu virus was first isolated from a pig in 1930.
2. Can it hurt me?
Influenza viruses infect pigs (swine), birds, humans and a few other species. Most strains of influenza are quite restricted in the host they will infect but occasionally jump from one species to another. Swine flu infects pigs but is also capable of infecting humans.
3. Will there be a swine flu pandemic?
It’s too early to say. Scientists are carefully recording the spread of the current epidemic to see how easily this virus is capable of spreading from person to person. World Health Organization (WHO) Director-General Margaret Chan says the present outbreak “has pandemic potential” but that “it is too early to say whether a pandemic will actually occur”.
Update: This outbreak is now officially a pandemic.
4. How many people have been affected by swine flu?
The number is growing – click here for the latest news.
5. Is there any treatment for swine flu?
Vaccines are available against H1N1 influenza but it is not known how effective they are against this strain. WHO says the virus appears to be susceptible to the influenza drug Tamiflu (oseltamivir), and Relenza (zanamivir). It is not known if resistance to these drugs will occur.
6. How does swine flu spread?
Influenza viruses are transmitted through coughing or sneezing by people infected with the virus. People may become infected by touching something with the virus on it and then touching their mouth or nose, so frequent hand washing is a good idea. You cannot get swine influenza from eating cooked pork or pork products.
7. Has swine flu infected humans before?
Sporadic human infections with swine flu occur regularly but not frequently, e.g. one or two a year in the USA. Most commonly, these cases occur in persons with direct exposure to pigs. There are a few previous cases of one person transmitting swine flu to others.
8. What are the symptoms of swine flu?
The symptoms of swine flu in people are similar to the symptoms of regular influenza, including fever, lethargy, lack of appetite and coughing. Some people with swine flu also have reported runny nose, sore throat, nausea, vomiting and diarrhea.
9. Should I travel to Mexico / the USA?
The World Health Organization (WHO) is not presently advising against travel to Mexico or the USA. National governments may be offering different advice (check locally). Travellers to affected areas are advised to consult a doctor immediately if they show signs of flu-like symptoms.
10. More information:
11. Are we all going to die?
Probably not. Every year many thousands of people around the world die as a result of influenza, a fact which goes largely unreported. The number of deaths increases in epidemic years. Pandemics (worldwide epidemics) occur unpredictably every 10-30 years. Millions of people die, billions survive.
Update: 10 more things you should know about H1N1 (swineflu)
How influenza pandemics get started
Thursday, April 23rd, 2009
H5, H7, and H9 avian influenza subtypes top the World Health Organization’s list of strains with the greatest pandemic potential. A transition from avian-like 2,3-linked sialic acid (SA2,3) receptors to human-like 2,6-linked sialic acid (SA2,6) receptors appears to be a crucial step for avian influenza viruses to replicate efficiently and transmit in humans. An increasing number of contemporary avian H9N2 viruses contain leucine (L) at position 226 in the hemagglutinin (HA) receptor-binding site (RBS), supporting the preferential binding to SA2,6 receptors and the ability to replicate efficiently in human respiratory epithelial cells and in the ferret model, an in vivo model which closely resembles human airway epithelium and clinical infection. Since the mid-1990’s, H9N2 influenza viruses have become endemic in poultry throughout Eurasia and have occasionally transmitted to humans and pigs. In addition to possessing human virus-like receptor specificity, avian H9N2 viruses induce typical human flu-like illness, which can easily go unreported, and therefore have the opportunity to circulate, undergo reassortment, and increase in transmissibility.
Seroepidemiological studies in Asia suggest that the incidence of human H9N2 infections could be more prevalent than what has been reported and possible human-to-human transmission cannot be completely excluded. These direct infections with avian H9N2 confirm that interspecies transmission of H9N2 from avian species to mammalian hosts occurs and it is not uncommon. Reassortment between the current human epidemic strain and an avian virus of a different subtype is postulated to generate the next pandemic strain. Given the receptor specificity of avian H9N2 viruses and their repeated introduction into humans, as recent as December 2008, the opportunity for their reassortment and/or adaptation for human-to-human transmission is ever present. However the question remains what is missing for the H9N2 virus to transmit from human-to-human and possibly lead to the next pandemic.
A new study describes respiratory droplet transmission of an avian–human H9N2 influenza virus in ferrets and pinpoints the minimal changes necessary for respiratory droplet transmission in this model. After only 10 passages of nasal washes researchers were able to establish infection and sustain respiratory droplet transmission that was reproducible in multiple studies. This adaptation required only 5 amino acid changes in the entire influenza virus genome, implying that little is needed for currently circulating avian H9N2 viruses to transmit human-to-human following reassortment with a human strain. Studies to identify the minimal changes necessary indicated three changes in the surface HA and NA as the key point mutations essential for respiratory droplet transmission. The scientists also identified and located a change that dramatically alters the antigenicity of the virus, bringing to light the inherent limitations in the selection of vaccine seed stocks for avian H9N2 viruses and the possible inefficiency regarding the seed stock selection of other avian influenza strains. Whether these changes can affect transmission phenotypes of additional avian H9N2 strains and possibly other influenza subtypes, most notably H5 and H7, remains to be determined.
Minimal molecular constraints for respiratory droplet transmission of an avian–human H9N2 influenza A virus. PNAS USA April 20, 2009
Pandemic influenza requires interspecies transmission of an influenza virus with a novel hemagglutinin (HA) subtytpe that can adapt to its new host through either reassortment or point mutations and transmit by aerosolized respiratory droplets. Two previous pandemics of 1957 and 1968 resulted from the reassortment of low pathogenic avian viruses and human subtypes of that period; however, conditions leading to a pandemic virus are still poorly understood. Given the endemic situation of avian H9N2 influenza with human-like receptor specificity in Eurasia and its occasional transmission to humans and pigs, we wanted to determine whether an avian–human H9N2 reassortant could gain respiratory transmission in a mammalian animal model, the ferret. Here we show that following adaptation in the ferret, a reassortant virus carrying the surface proteins of an avian H9N2 in a human H3N2 backbone can transmit efficiently via respiratory droplets, creating a clinical infection similar to human influenza infections. Minimal changes at the protein level were found in this virus capable of respiratory droplet transmission. A reassortant virus expressing only the HA and neuraminidase (NA) of the ferret-adapted virus was able to account for the transmissibility, suggesting that currently circulating avian H9N2 viruses require little adaptation in mammals following acquisition of all human virus internal genes through reassortment. Hemagglutinin inhibition (HI) analysis showed changes in the antigenic profile of the virus, which carries profound implications for vaccine seed stock preparation against avian H9N2 influenza. This report illustrates that aerosolized respiratory transmission is not exclusive to current human H1, H2, and H3 influenza subtypes.
Related:
- The Biology of Influenza
- Influenza pandemic – when?
- The Pathogenicity of Pandemic Influenza Viruses
- H5N1 and 1918 pandemic influenza virus infection and the lungs
The Pathogenicity of Pandemic Influenza Viruses
Thursday, February 5th, 2009Dr. Peter Palese describes how reconstructing the extinct 1918 pandemic influenza virus by reverse genetics can help us better understand molecular basis of virulence and the mechanisms by which pandemic influenza viruses are transmitted.
The poultry industry in Great Britain: transmission routes for a potential avian influenza virus epidemic
Thursday, October 30th, 2008
The UK commercial poultry industry is an important industry to the British government, the consumer and farmers alike. Worth an estimated £3.4 billion at retail value, producing over 174 million birds for consumption per year, poultry diseases are of widespread interest, both from the point-of-view of understanding different poultry farming methods, and in terms of studying the potential impact of different diseases on poultry. However, our knowledge of how poultry farms in the UK are connected to each other by the movement of people and equipment is more limited. This is essential for effective prevention and control for potential outbreaks of diseases transmitted by the movement of people and equipment between farms within the commercial poultry industry. Diseases spread in such a way include avian influenza viruses (AIV), Newcastle disease virus, Salmonella and Campylobacter species.
An epidemic of any poultry disease with high mortality or which is zoonotic, such as AIV, would result in the culling of significant numbers of birds, as seen in the Netherlands in 2003 and Italy in 2000. Such an epidemic would cost the UK government millions of pounds in compensation costs, with further economic losses through reduction of international and UK consumption of British poultry. In order to better inform policy advisers and makers on the potential for a large epidemic in the UK, we investigate the role that interactions amongst premises within the British commercial poultry industry could play in promoting an AIV epidemic, given an introduction of the virus in a specific part of poultry industry in the UK.
Poultry premises using multiple slaughterhouses lead to a large number of premises being potentially connected, with the resultant potential for large and sometimes widespread epidemics. Catching companies can also potentially link a large proportion of the poultry population. Critical to this is the maximum distance traveled by catching companies between premises and whether or not between-species transmission could occur within individual premises. Premises closely linked by proximity may result in connections being formed between different species and or sectors within the industry.
Even quite well-contained epidemics have the potential for geographically widespread dissemination, potentially resulting in severe logistical problems for epidemic control, and with economic impact on a large part of the country. Premises sending birds to multiple slaughterhouses or housing multiple species may act as a bridge between otherwise separate sectors of the industry, resulting in the potential for large epidemics. Investment into further data collection and analyses on the importance of industry structure as a determinant for spread of AIV would enable us to use the results from this study to contribute to policy on disease control.
Related:
- H5N1 influenza is no longer bird flu
- Negative sense RNA viruses
- Human Infections with Avian Influenza H5N1 Viruses
- Media coverage affects how people perceive the threat of disease
New research on flu vaccination
Tuesday, October 28th, 2008
As this year’s flu season gets underway in the northern hemisphere, new research finds that when it comes to flu vaccination, more appears to be better. Two new studies published in the open access journal PLoS Medicine show that increasing the number of people vaccinated against influenza can decrease the burden of the disease, and not just in the individuals receiving the vaccine.
Targeted vaccination programs, in which flu vaccine is recommended for particular groups at high risk of spreading or experiencing complications of influenza, are commonly implemented. In contrast, the Canadian province of Ontario initiated a universal immunization program in 2000, in which flu vaccination is promoted and provided free of charge to everyone over the age of 6 months. The first study evaluated the effect of this universal immunization program on influenza-associated health outcomes. The researchers analyzed national and provincial data from 1997 to 2004, to compare changes in Ontario’s flu outcomes before and after introduction of universal vaccination with outcomes in other provinces, which continued targeted vaccination programs. They found that, compared with other Canadian provinces, Ontario’s universal vaccination program was associated with reductions in influenza outcomes including flu-related deaths, hospitalizations, and visits to emergency departments and doctors’ offices. The results did suggest, however, that increasing immunization rates may not be as effective in reducing mortality and health care use in older people, particularly those over 75 years of age, compared to younger people. However, even with enhanced access to free flu vaccines in Ontario, only an estimated average of 38% of the overall household population reported receiving them, suggesting that protection of older people by higher immunization rates of younger contacts who might expose them to influenza may still be of benefit.
The second study further investigated the concept of herd immunity, by which immunization of some individuals protects the overall population by reducing exposure of those who are not immunized. Using a mathematical model to simulate spread of influenza in nursing homes, researchers found that increasing the number of health care staff who are vaccinated can protect additional patients from influenza. They calculated that increasing the proportion of vaccinated health care workers from zero to 100% in a 30-bed nursing home department would reduce patient infections by about 60%, and that vaccinating seven health care workers would on average prevent one patient from getting influenza. They also found that no level of health care worker vaccination guarantees complete herd immunity, suggesting that even at high levels of immunization, increasing the number of nursing home staff who are vaccinated against flu each year will further reduce risk to patients. The authors also note that random variation, which occasionally leads to large outbreaks, limits the ability of small vaccination trials to assess the actual relationship between health-care worker vaccination and patient risk of influenza.
