What happened in 1957 and 1968?

[Sally Furniss]

What happened in 1957 and 1968?

In May 1957 the Asian influenza was identified in Singapore. By May 1958 it had spread worldwide. Infection rates were reported to range from 20-70 percent but fatalities were low ranging from 1 in 2000 to 1-10,000 infections. In New Zealand the pandemic began in Wellington in August 1957. The most at risk were people aged from 10-30 years. A second wave hit in late 1959. In July 1968 a new type emerged in Hong Kong - it reached New Zealand in early 1969. Sporadic cases were reported during New Zealand's summer and autumn and it reached epidemic levels in June and July.

 

[Sally Furniss]

Re: What happened in 1957 and 1968?

1957: Asian Influenza (H2N2) <hr style="color: rgb(209, 209, 225);" size="1"> <!-- / icon and title --> <!-- message --> History
[FONT=Arial, Helvetica, sans-serif]Influenza Pandemics of the 20th Century[/FONT]

Edwin D. Kilbourne*
*New York Medical College, Valhalla, New York, USA

[FONT=Arial, Helvetica, sans-serif]1957: Asian Influenza (H2N2)[/FONT]

After the influenza pandemic of 1918, influenza went back to its usual pattern of regional epidemics of lesser virulence in the 1930s, 1940s, and early 1950s. With the first isolation of a virus from humans in 1933 (5), speculation began about the possible role of a similar virus in 1918. However, believing that this could have been the case was difficult until the pandemic of 1957. This was the first time the rapid global spread of a modern influenza virus was available for laboratory investigation. With the exception of persons >70 years of age, the public was confronted by a virus with which it had had no experience, and it was shown that the virus alone, without bacterial coinvaders, was lethal (6).
[FONT=Arial, Helvetica, sans-serif]First Recognition of the Pandemic[/FONT]

In 1957, worldwide surveillance for influenza was less extensive than it is today. However, attentive investigators in Melbourne, London, and Washington, DC soon had the virus in their laboratories (7) after the initial recognition of a severe epidemic, followed by the publication in The New York Times of an article in 1957 describing an epidemic in Hong Kong that involved 250,000 people in a short period (8). Three weeks later, a virus was recovered from the outbreak and sent to Walter Reed Army Institute for Research in Washington, DC for study.
[FONT=Arial, Helvetica, sans-serif]Nature of the Virus[/FONT]

The virus was quickly recognized as an influenza A virus by complement fixation tests. However, tests defining the HA antigen of the virus showed it to be unlike any previously found in humans. This was also true for the neuraminidase (NA) antigen. The definitive subtype of the Asian virus was later established as H2N2. The new virus had high sialidase/neuraminidase activity, and this activity was more stable than that of earlier strains. Different strains of the Asian virus also differed markedly with respect to sensitivity to either antibody neutralization or nonspecific inhibitors of hemagglutination (9). In animal studies, the new H2N2 viruses did not differ in their virulence characteristics from earlier influenza A subtypes. Viral isolates from the lungs of patients with fatal cases showed no discernible differences from those from throat washing isolates of patients without pulmonary involvement within a small circumscribed hospital outbreak (10).
[FONT=Arial, Helvetica, sans-serif]Primary Influenza Virus Pneumonia[/FONT]

Although secondary or concomitant bacterial infections of the lung were found to be a prominent feature of fatal cases in 1918 when a specific etiologic agent was sought (4), many cases of rapid death and lung consolidation or pulmonary edema occurred in which bacterial infection could not be demonstrated. As influenza persisted as an endemic disease with regional recurrences after the pandemic, lives continued to be occasionally claimed by abacterial pneumonia.
With the arrival of Asian influenza in 1957, the sheer number of cases associated with pandemicity again brought the phenomenon of primary influenza virus pneumonia to the attention of physicians in teaching hospitals. In contrast to the observations in 1918, underlying chronic disease of the heart or lungs was found in most of these patients, although deaths of previously healthy persons were not uncommon. In the case of carefully studied patients at the New York Hospital, rheumatic heart disease was the most common antecedent factor, and women in the third trimester of pregnancy were among those vulnerable (11).
[FONT=Arial, Helvetica, sans-serif]Response to Vaccination in an Unprimed Population[/FONT]

The pandemic of 1957 provided the first opportunity to observe vaccination response in that large part of the population that had not previously been primed by novel HA and NA antigens not cross-reactive with earlier influenza A virus antigens. As summarized by Meiklejohn (12) at an international conference on Asian influenza held 3 years after the 1957 onslaught of H2N2, more vaccine was required to initiate a primary antibody response than with the earlier H1 vaccines (almost always observed in heterovariant primed subjects). In 1958, 1959, and 1960 (as recurrent infections occurred), mean initial antibody levels in the population increased (i.e., subjects were primed) and response to vaccination was more readily demonstrated. Divided doses given at intervals of <4 weeks were more beneficial than a single injection. Less benefit was derived from this strategy as years passed. Intradermal administration of vaccine provided no special advantage over the conventional subcutaneous/intramuscular route, even when the same small dose was given (13).
[FONT=Arial, Helvetica, sans-serif]Nature of Endemic H2N2 Postpandemic Infection[/FONT]

The Asian influenza experience provided the first opportunity to study how the postpandemic infection and disease into an endemic phase subsided. In studies conducted in separate and disparate populations (14), the populations compared were Navajo school children and New York City medical students. In both groups, subclinical infections occurred each year during the 3-year study period, and clinically manifested infections decreased in conjunction with an increasing level of H2N2-specific hemagglutination inhibition antibody.
A decreasing incidence of clinically manifested cases can be ascribed either to the increase in antibody levels in the community or to a change in the intrinsic virulence of the virus. Therefore, the nature of the disease during the endemic period is important to define. A study (15) in 1960 of hospitalized patients with laboratory-confirmed infections demonstrated a spectrum of disease from uncomplicated 3-day illnesses to fatal pneumonia, all in the absence of discernible epidemic influenza in the community (15). Asian (H2N2) virus was destined for short survival in the human population and disappeared only 11 years after its arrival. It was supplanted by the Hong Kong (H3N2) subtype.
http://www.cdc.gov/ncidod/EID/vol12no01/05-1254.htm#asi

 

[Sally Furniss]

Re: What happened in 1957 and 1968?

1968: Hong Kong Influenza (H3N2) <hr style="color: rgb(209, 209, 225);" size="1"> <!-- / icon and title --> <!-- message --> <!-- #BeginEditable "content_area_2" --> History
[FONT=Arial, Helvetica, sans-serif]Influenza Pandemics of the 20th Century[/FONT]

Edwin D. Kilbourne*
*New York Medical College, Valhalla, New York, USA

[FONT=Arial, Helvetica, sans-serif]
1968: Hong Kong Influenza (H3N2)[/FONT]

As in 1957, a new influenza pandemic arose in Southeast Asia and acquired the sobriquet Hong Kong influenza on the basis of the site of its emergence to western attention. Once again, the daily press sounded the alarm with a brief report of a large Hong Kong epidemic in the Times of London. A decade after the 1957 pandemic, epidemiologic communication with mainland China was even less efficient than it had been earlier.
As this epidemic progressed, initially throughout Asia, important differences in the pattern of illness and death were noted. In Japan, epidemics were small, scattered, and desultory until the end of 1968. Most striking was the high illness and death rates in the United States following introduction of the virus on the West Coast. This experience stood in contrast with the experience in western Europe, including the United Kingdom, in which increased illness occurred in the absence of increased death rates in 1968?1969 and increased death rates were not seen until the following year of the pandemic.
Since the Hong Kong virus differed from its antecedent Asian virus by its HA antigen, but had retained the same (N2) NA antigen (16), researchers speculated that its more sporadic and variable impact in different regions of the world were mediated by differences in prior N2 immunity (16?19). Therefore, the 1968 pandemic has been aptly characterized as "smoldering" (19). Further evidence for the capacity of previous N2 experience to moderate the challenge of the Hong Kong virus was provided by Eickhoff and Meiklejohn (20), who showed that vaccination of Air Force cadets with an H2N2 adjuvant vaccine reduced subsequent influenza from verified H3N2 virus infection by 54%.
The amelioration of H3N2 virus infection by NA immunity alone is all the more remarkable because of the capacity of the virus to kill, as occurred in 1918 and 1957, although a broader spectrum of disease severity was apparent in 1968 than in 1957 (15). Although not necessarily an indication of virulence, cross-species transmission of the virus was observed (21). Thirty-seven years later, the H3N2 subtype still reigns as the major and most troublesome influenza A virus in humans.
http://www.cdc.gov/ncidod/EID/vol12no01/05-1254.htm#asi

 

[KC]

Re: What happened in 1957 and 1968?

Interesting topic worth discussion....NA antigen immunity or resistance.

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> Influenza Report 2006 http://influenzareport.com/influenzareport2006.pdf

1968 Pandemic:

“The 1968 pandemic, was also a mild pandemic. The mortality impact was not even particularly severe compared to the severe epidemic in 1967.1968 (the last H2N2 epidemic), as well as two severe H3N2 epidemics in 1975.1976, and in 1980.1981 (Simonsen 2004). The death toll has been estimated to have been around 1 million, and in the United States, nearly 50 percent of all influenza-related deaths occurred in the younger population under 65 years of age. Sero-archaeological studies showed that most individuals aged 77 years or older, had H3 antibodies before they were exposed to the new pandemic virus (Dowdle 1999) and that pre-existing anti-H3 antibodies might have protected the elderly (> 77 years old) during the 1968
H3N2 pandemic.” (Influenza Report 2006, p. 22)

H5N1:

“Until now, the disease has predominantly affected children and young adults. Of 116 patients for whom demographical data had been published on the WHO Website from December 2003 until 9 February 2006, 50 % were 16 years old or younger, 75 % were younger than 30 years, and 90 % were younger than 40 years old (Promed 20060211.0463). The reason for this age distribution (exposure risk, disease reporting bias, intrinsic host issues, etc.) is unclear. Likewise, it is not known whether, and to what extent, genetic composition plays a role in the susceptibility and resistance to infection with H5N1 influenza virus (Promed 20060216.0512).” (Influenza Report 2006, p.23)

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> Influenza Report 2006http://influenzareport.com/ir/figures/ad060406.htm

6 April 2006

"An analysis of demographic data published by WHO shows the following age distribution of human H5N1 influenza cases (n=144). 50% of cases were 17 years or younger; 75% of cases were 29 years or younger; 90% of cases were 37 years or younger. Most patients were born after 1968."

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> 1968: Hong Kong Influenza (H3N2)

History

Influenza Pandemics of the 20th Century

Edwin D. Kilbourne*
*New York Medical College, Valhalla, New York, USA

..."As this epidemic progressed, initially throughout Asia, important differences in the pattern of illness and death were noted. In Japan, epidemics were small, scattered, and desultory until the end of 1968. Most striking was the high illness and death rates in the United States following introduction of the virus on the West Coast. This experience stood in contrast with the experience in western Europe, including the United Kingdom, in which increased illness occurred in the absence of increased death rates in 1968–1969 and increased death rates were not seen until the following year of the pandemic."

"Since the Hong Kong virus differed from its antecedent Asian virus by its HA antigen, but had retained the same (N2) NA antigen (16), researchers speculated that its more sporadic and variable impact in different regions of the world were mediated by differences in prior N2 immunity (16–19). Therefore, the 1968 pandemic has been aptly characterized as "smoldering" (19). Further evidence for the capacity of previous N2 experience to moderate the challenge of the Hong Kong virus was provided by Eickhoff and Meiklejohn (20), who showed that vaccination of Air Force cadets with an H2N2 adjuvant vaccine reduced subsequent influenza from verified H3N2 virus infection by 54%...."

 

[KC]

Re: What happened in 1957 and 1968?

> U.S. Health and Human Services http://www.hhs.gov/nvpo/pandemics/flu3.htm

1968: Hong Kong Flu

In early 1968, the Hong Kong influenza pandemic was first detected in Hong Kong. The first cases in the U.S. were detected as early as September of that year, but illness did not become widespread in the U.S. until December. Deaths from this virus peaked in December 1968 and January 1969. Those over the age of 65 were most likely to die. The same virus returned in 1970 and 1972. The number of deaths between September 1968 and March 1969 for this pandemic was 33,800, making it the mildest pandemic in the 20th century.

There could be several reasons why fewer people in the U.S. died due to this virus. First, the Hong Kong flu virus was similar in some ways to the Asian flu virus that circulated between 1957 and 1968. Earlier infections by the Asian flu virus might have provided some immunity against the Hong Kong flu virus that may have helped to reduce the severity of illness during the Hong Kong pandemic. Second, instead of peaking in September or October, like pandemic influenza had in the previous two pandemics, this pandemic did not gain momentum until near the school holidays in December. Since children were at home and did not infect one another at school, the rate of influenza illness among schoolchildren and their families declined. Third, improved medical care and antibiotics that are more effective for secondary bacterial infections were available for those who became ill.

1977: Russian Flu Scare

In May 1977, influenza A/H1N1 viruses isolated in northern China, spread rapidly, and caused epidemic disease in children and young adults (< 23 years) worldwide. The 1977 virus was similar to other A/H1N1 viruses that had circulated prior to 1957. (In 1957, the A/H1N1 virus was replaced by the new A/H2N2 viruses). Because of the timing of the appearance of these viruses, persons born before 1957 were likely to have been exposed to A/H1N1 viruses and to have developed immunity against A/H1N1 viruses. Therefore, when the A/H1N1 reappeared in 1977, many people over the age of 23 had some protection against the virus and it was primarily younger people who became ill from A/H1N1 infections. By January 1978, the virus had spread around the world, including the United States. Because illness occurred primarily in children, this event was not considered a true pandemic. Vaccine containing this virus was not produced in time for the 1977-78 season, but the virus was included in the 1978-79 vaccine.

 

[KC]

Re: What happened in 1957 and 1968?

Proc Natl Acad Sci U S A. 1969 June; 63(2): 326?333.

INDEPENDENT VARIATION IN NATURE OF HEMAGGLUTININ AND NEURAMINIDASE ANTIGENS OF INFLUENZA VIRUS: DISTINCTIVENESS OF HEMAGGLUTININ ANTIGEN OF HONG KONG/68 VIRUS*J. L. Schulman and E. D. Kilbourne

DEPARTMENT OF PUBLIC HEALTH, CORNELL UNIVERSITY MEDICAL COLLEGE
DEPARTMENT OF MICROBIOLOGY, MOUNT SINAI SCHOOL OF MEDICINE

* This investigation was conducted in part under the auspices of the Commission on Influenza, Armed Forces Epidemiological Board, and was supported in part by the U.S. Army Medical Research and Development Command, Department of the Army, under research contract DA-49-193-MD-2795; in part by USPHS research grant AI-09304 from the National Institutes of Allergy and Infectious Diseases; and in part by the Health Research Council of the City of New York under contract U-1023.

Abstract

Antigenic variations of the two virus-coded surface proteins of influenza virus?hemagglutinin and neuraminidase?were examined in seven strains of influenza A2 virus (including the Hong Kong/68 strain) isolated from 1957 to 1968. Changes in the two antigens were found to occur independently in nature, resulting in new viruses which differ from older strains more with respect to one antigen than the other. The Hong Kong/68 strain is markedly different from previous A2 strains in its hemagglutinin antigen but possesses neuraminidase indistinguishable antigenically from that of recent strains. Immunization experiments in mice provided evidence that only the neuraminidase component of an earlier A2 strain provided protection against Hong Kong virus challenge.

Segregation of hemagglutinin and neuraminidase antigens through recombination of each of the seven strains of influenza A2 virus with A0/NWS virus made it possible to investigate antigenic variation of the two dissociated surface proteins independently in a common plaque assay system. Comparison of these hybrid viruses with the parent A2 strains provided evidence that all the cross-reactivity of the Hong Kong strain with previous A2 viruses is explicable on the basis of its similar neuraminidase component. It is proposed that the taxonomy of influenza A viruses must take into account differences in neuraminidase as well as hemagglutinin antigens.

Full Paper: http://www.pubmedcentral.gov/picrender.fcgi?artid=223568&blobtype=pdf

 

[KC]

Re: What happened in 1957 and 1968?

> Luk et al. Mortality During the 1918 Influenza Pandemic
http://www.journals.uchicago.edu/CID/journal/issues/v33n8/001674/001674.text.html

"The original purpose of our study was to examine the unusual W-shaped mortality curve associated with the 1918 influenza pandemic and possibly explain the peak in mortality among individuals aged 2040 years. We plotted age-specific excess mortality instead of total mortality for the 1918 pandemic using a 5-year baseline. For comparison, we also graphed excess mortality curves for the 1957 and 1968 pandemics using 5-year baselines. The 1957 and 1968 curves exhibited the usual U-shaped curve, with high excess mortality among infants and the elderly population relative to young adults. The 1918 curve, however, presented unexpected results. A peak in excess mortality among infants and young adults was seen, but the expected W shape did not result. We instead found negative excess mortality among elderly individuals, suggesting that this group was exposed, at an earlier date, to an influenza strain similar to the so-called Spanish influenza (H1N1) strain."

 

[AlaskaDenise]

Re: What happened in 1957 and 1968?

Lobo:

I believe that "negative excess mortality among elderly" is assumed due to an 1889 flu (& some other nearby years). But there are no samples to test for it's hemmaglutinin or neurominidase.

Are you saying that the 1918 elderly advantage might be because of a previously circulating HxN1? If so, do you think the currently circulating H1N1 should help protect people from H5N1 who have had an H1N1 infection?

.

 

[KC]

Re: What happened in 1957 and 1968?

AD,

I am pretty well convinced that H5N1 is acting like the 1918 H1N1 virus. There is something associated with it that causes a cytokine storm and extensive hemorrhagic organ damage to the youngest people while sparing the oldest.

Dr. Taubenberger wrote something about this in 2001 (I believe that was the year). I'll have to look up the paper again. I didn't want to post it earlier because he has changed some of his views, after further research, since the paper was published.

As far as being exposed to an HxN1 virus protecting people?... Who knows. I have been spooling through lots of research papers today to find out why the young are dying and the old are surviving. The arguement that the young have the healthiest immune systems is poor at best to me. There is something that the current research is missing, or not learning from or recognizing from the past. I firmly believe that something other than the young peoples "healthy immune system" is the reason. The older peoples immune systems just "recognise" and "react" appropriately to the new virus.... they have had some form of contact with something associated with the virus (who knows what), in some way, to achieve immunity, partial immunity, or an appropriate immune reaction.

Here is where I began today: (Thanks AnneZ)

Schulman JL, Kilbourne ED. Independent variation in nature of the hemagglutinin and neuraminidase antigens of influenza virus: distinctiveness of the hemagglutinin antigen of Hong Kong-68 virus. Proc Natl Acad Sci U S A. 1969;63:326?33.

Stuart-Harris C. Epidemiology of influenza in man. Br Med Bull. 1979;35:3?8.

Monto AS, Kendal AP. Effect of neuraminidase antibody on Hong Kong influenza. Lancet. 1973;1:623?5.

Viboud C, Grais RF, Lafont BA, Miller MA, Simonsen L; Multinational Influenza Seasonal Morbidity Study Group. Multinational impact of the 1968 Hong Kong pandemic: evidence for a smoldering pandemic. J Infect Dis. 2005;192:223?48.

 

[KC]

Re: What happened in 1957 and 1968?

KC:

I believe that "negative excess mortality among elderly" is assumed due to an 1889 flu (& some other nearby years). But there are no samples to test for it's hemmaglutinin or neurominidase.

Are you saying that the 1918 elderly advantage might be because of a previously circulating HxN1? If so, do you think the currently circulating H1N1should help protect people from H5N1 who have had an H1N1 infection?

.

AD,

I was listening to Dr. Drew Pinski on the radio today while at work. He hypothesised (re: 1918 N1N1 and emerging H5N1) that there could be some form of immunity but there wasn't any documented or researched pandemics of influenza in the 19th century. He went on to say, "I don't know what the virus in 1918 was... I believe it was also H5N1"... After that statement, the remainder of his answer to the caller was suspect.

I believe (I am not an expert) that we have long overlooked the importance on virulence (or lack of virulence) that the NA antigen has on emerging HPAI and LPAI viruses. I also believe that we are overlooking the effects that emerging viruses have when they "co-mingle" with existing endemic, non AI viruses. I base my beliefs on my personal and non-professional secondary research of the past and applying that knowledge to critically analyze current research and trends.

"Those who cannot learn from history are doomed to repeat it." (One of many versions of his famous quote)...George Santayana

The reason a knowledge of history is needed in current and future research. (Click Here) (Jone Johnson Lewis, wisdomquotes.com)

 

[KC]

Re: What happened in 1957 and 1968?

The reason a knowledge of history is needed in current and future research. (Click Here)

Some selected quotes from the above:

Adrienne Rich:
"False history gets made all day, any day,
the truth of the new is never on the news."

Alex Haley:
"In every conceivable manner, the family is link to our past, bridge to our future."

David Ben Gurion:
"Anyone who believes you can't change history has never tried to write his memoirs."

Etienne Gilson:
"History is the only laboratory we have in which to test the consequences of thought."

George Wilhelm Hegel:
"What experience and history teach is this -- that people and governments never have learned anything from history, or acted on principles."

Goethe:
"Patriotism ruins history."

Winston Churchill:
"History will be kind to me for I intend to write it."

 

[KC]

Re: What happened in 1957 and 1968?

Some quotes from this discussion:

Interesting topic worth discussion....NA antigen immunity or resistance.

1968 Pandemic:
“The 1968 pandemic, was also a mild pandemic. The mortality impact was not even particularly severe compared to the severe epidemic in 1967.1968 (the last H2N2 epidemic), as well as two severe H3N2 epidemics in 1975.1976, and in 1980.1981 (Simonsen 2004). The death toll has been estimated to have been around 1 million, and in the United States, nearly 50 percent of all influenza-related deaths occurred in the younger population under 65 years of age. Sero-archaeological studies showed that most individuals aged 77 years or older, had H3 antibodies before they were exposed to the new pandemic virus (Dowdle 1999) and that pre-existing anti-H3 antibodies might have protected the elderly (> 77 years old) during the 1968
H3N2 pandemic.” (Influenza Report 2006, p. 22)

1977: Russian Flu Scare

In May 1977, influenza A/H1N1 viruses isolated in northern China, spread rapidly, and caused epidemic disease in children and young adults (< 23 years) worldwide. The 1977 virus was similar to other A/H1N1 viruses that had circulated prior to 1957. (In 1957, the A/H1N1 virus was replaced by the new A/H2N2 viruses).

(... and in the 1918/19/20 virus but somehow recombined?). It (1977) was never termed a pandemic because it only had a range of morbidity and mortality from the 0-23 years of age range even though it spread worldwide.

I believe that "negative excess mortality among elderly" is assumed due to an 1889 flu (& some other nearby years). But there are no samples to test for it's hemmaglutinin or neurominidase.

Are you saying that the 1918 elderly advantage might be because of a previously circulating HxN1? If so, do you think the currently circulating H1N1 should help protect people from H5N1 who have had an H1N1 infection?

I believe (I am not an expert) that we have long overlooked the importance on virulence (or lack of virulence) that the NA antigen has on emerging HPAI and LPAI viruses. I also believe that we are overlooking the effects that emerging viruses have when they "co-mingle" with existing endemic, non AI viruses. I base my beliefs on my personal and non-professional secondary research of the past and applying that knowledge to critically analyze current research and trends.

"Those who cannot learn from history are doomed to repeat it." (One of many versions of his famous quote)...George Santayana

Now, my amateur research on history has evolved to try to understand the history behind NS proteins (particularly NS1) and how they (NS proteins) have evolved throughout history to increase virulense of various viruses, and/or resistance to spread and morbidity and mortality, and how they relate to past exposures of similiar, if not identical, viral proteins.

 

[Sally Furniss]

Re: What happened in 1957 and 1968?

Summary in layman's terms, Correct me if I am wrong.
The 1977 Russian flu was H1N1
H5N1 is hitting people born after mid 1970's
Therefore the N in Russian flu and bird flu may be similar and may be giving some protection against H5N1 to persons who had the Russian Flu.

 

[KC]

Re: What happened in 1957 and 1968?

Now, my amateur research on history has evolved to try to understand the history behind NS proteins (particularly NS1) and how they (NS proteins) have evolved throughout history to increase virulense of various viruses, and/or resistance to spread and morbidity and mortality, and how they relate to past exposures of similiar, if not identical, viral proteins.

AnneZ, good question.

Therefore the N in Russian flu and bird flu may be similar and may be giving some protection against H5N1 to persons who had the Russian Flu.

Seems most research has been on the H side of the equation (ability to spread) rather than the N side (virulense and adaptability to recombine with viral properties of other viruses). Obviously, more research is needed.

 

[Sonny]

Re: What happened in 1957 and 1968?

KC, If you're interested in how NS1 influences host imunity to its advantage, then you might also be interested in reading about the recently discovered virus protien PB1-F2. Studies have shown it causes cell death by targeting the mitocondria. Its almost never found in swine isolates. Its not required for virus replication or infection. It targets immune cells, the monocytes. It's present in the H5N1 viruses

Now, my amateur research on history has evolved to try to understand the history behind NS proteins (particularly NS1) and how they (NS proteins) have evolved throughout history to increase virulense of various viruses, and/or resistance to spread and morbidity and mortality, and how they relate to past exposures of similiar, if not identical, viral proteins

.

 

[KC]

Re: What happened in 1957 and 1968?

Thank you Sonny. I've been away for the last week and will take a look at that.