New York Times, July 17, 2005
Kilbourne in 1976 (1) noted that pandemics of influenza occur every 11 years


Hepatitis C virus (HCV) infection causes chronic liver diseases and is a global public health problem. Detailed analyses of HCV have been hampered by the lack of viral culture systems. Subgenomic replicons of the JFH1 genotype 2a strain cloned from an individual with fulminant hepatitis replicate efficiently in cell culture. Here we show that the JFH1 genome replicates efficiently and supports secretion of viral particles after transfection into a human hepatoma cell line (Huh7).
Production of infectious hepatitis C virus in tissue culture from a cloned viral genome
https://www.nature.com/articles/nm1268
Translation:"We cloned a virus and can grow it now if we use human cancer cells".

Illustration of the various dynamic and constant solar effects on Earth. The two solar constants, sunlight and solar wind, takes 8 minutes and 4 days, respectively, to reach Earth. Arrival times of dynamic solar events such as Flares, solar energetic particles and CMEs, are approximated and range from immediate effect to several days. - NASA
Major flu pandemics struck right after both world wars and in 1936, 1957, 1968, 1979.
  • The 1977–1978 Russian flu epidemic was caused by strain Influenza A/USSR/90/77 (H1N1).[1]
  • 2009 A total of 74 countries are affected. 18,500 deaths.
  • 1976 Fort Dix, USA, 1 dead, 13 ill. Vaccinations proceed which kill 32.
  • 1977 Russia and China[2]

    [1]"Because of a striking similarity in the viral RNA of both strains – one which is unlikely to appear in nature due to antigenic drift – it was speculated that the later outbreak was due to a laboratory incident in Russia or Northern China, though this was denied by scientists in those countries." - Wikipedia

    [2]"The 1977-1978 influenza epidemic was probably not a natural event, as the genetic sequence of the virus was nearly identical to the sequences of decades-old strains"

    "There are multiple potential explanations that may explain the viral resurgence, but the possibility that the epidemic was the result of a laboratory accident has recently gained currency in discussions about the biosafety risks of gain-of-function (GOF) in- fluenza virus research and has been used as an argument for why this research should not be performed. GOF studies aim to better understand disease pathways, but they have been controversial because they involve enhancing viral traits, such as pathogenicity or transmissibility, prompting biosafety concerns."

    " In 1976, the swine H1N1 epizootic influenza virus infected 230 soldiers at Fort Dix, NJ, causing severe respiratory illness in 13 and one death (12). Edwin Kilbourne and others led a campaign that resulted in President Gerald Ford announcing a program to inoculate everyone in the United States against swine flu, and the concomitant production of 150 million doses of influenza vaccine. However, the program was halted soon after, as it became clear that A/New Jersey/ 1976 was not spreading outside the basic training group. It is possible that an archival H1N1 strain from the early 1950s was used as a challenge virus to evaluate the efficacy of the H1N1 vaccines prepared in response to the 1976 swine flu outbreak. If this virus were not attenuated properly, it may have been able to spread and cause a global epidemic."

    "No single gene of the 1918 influenza virus accounts for its high degree of pathogenicity. Therefore, we are forced to conclude that the lethal effect is caused by many viral genes (polygenic). The definition of this profound lethality is that the resurrected 1918 virus is 100 times more lethal than other strains for experimental animals so-infected; it replicates in some instances to produce 39,000 more virus particles than other influenza strains, and it causes severe lung injury in mice and monkeys very similar to that in lungs from humans who died from the 1918–19 influenza virus infection. Further, unlike other influenza viruses, the 1918 resurrected virus is lethal when injected into chick embryos. Although many of its genes may participate in the virulence, both the hemagglutinin and polymerase genes likely play the dominant roles.

    "Other clues as to the virulence of the 1918 influenza virus have come from recent studies in monkeys (38). Infection of cynomologous monkeys with a contemporary influenza strain led to mild symptoms and minimal pathology in the lung. In contrast, the revived 1918 influenza virus spread rapidly through their lungs and was lethal. Particularly important was an outcome of 1918 influenza virus infection in which the monkeys’ immune systems went into overdrive causing an increased production of host proteins called cytokines. This immunopathologic effect is called a “cytokine storm.”" - VPH



    "The Reemergent 1977 H1N1 Strain and the Gain-of-Function Debate"
    http://mbio.asm.org/content/6/4/e01013-15.short