You may have recently heard about the new Chinese swine flu that has the potential to become a pandemic virus and wondered, what is happening? Have we crossed over into some new territory? The short answer: No.
With COVID-19 in the spotlight we tend to forget about other viruses. But, they have not gone into “suspended animation.” They continue to infect, change and follow their natural courses. As epidemiologists and public health practitioners, we continue to watch and track these viruses, as well as bacteria and parasites.
A new Influenza A virus strain was found in swine in China and has recently been found in humans (specifically, among Chinese farmworkers and slaughterhouse workers). After analyzing influenza virus samples from pigs over a 7-8 year period, scientists in China identified the new strain of Influenza A and found that it has many of the characteristics of a pandemic virus. It appears to be a mixture of the 2009 swine flu virus and another strain. Named the “G4” strain of H1N1, its inner core is an avian (bird) virus (to which humans have no immunity) with bits of mammalian virus genes mixed in. The scientists cultured this virus with human cells and found that G4 easily attached to human cells that line human airways. Although they found evidence of human infection, they only reported two cases of people who were actively infected and found no evidence of person-to-person transmission.
As a rule, viruses that primarily infect swine, and occasionally infect humans, do not easily spread from person-to-person. However, as we saw in 2009, the primarily swine influenza virus underwent a transformation. It acquired the genes of two swine-origin viruses, one avian-origin virus and one human-origin virus. This mutated virus spread easily from person-to-person, and a pandemic started.
Could the G4 virus also mutate and spread among people?
To understand how and why all influenza viruses change so quickly and so often, consider that they all consist of separate RNA strands with no DNA. RNA viruses replicate rapidly, but lack the “proofreading” that DNA viruses contain – so they have high error rates when they make copies of themselves. That enhances the potential for new mutations/strains with new characteristics.
There are two main types of influenza viruses: Influenza A and Influenza B (Influenza C and D are rare and far less concerning). The many different subtypes of type A (or “strains”) differ because of changes in certain proteins on the surface of the virus (called hemagglutinin [H] and neuraminidase [N]). That is why type A viruses have names such as A(H1N1) whereby we refer to the type of H and N proteins they express. Since there are 18 different H proteins and 11 different N proteins, many different combinations of H and N proteins are possible. Fortunately, many of the possible combinations are unable to cause illness or even survive. Nonetheless, each combination represents a different influenza virus. The different subtypes of A undergo genetic mutations much more commonly than the two B types in existence. From each new mutation springs the possibility of an epidemic and a broader pandemic.
Influenza viruses change in a number of ways: 1) mutation (due to errors in copying), 2) jumping hosts, 3) reassortment (where strands of RNA from two different influenza viruses mix), and 4) recombination (where only partial RNA/gene strands from different influenza viruses mix). Changes result in altered infectivity/virulence.
“Host jumping” occurs when an influenza virus, without undergoing any genetic change, can infect a species different from its usual host. This is seen more commonly in some of the avian influenza viruses where very close and frequent contact may result in a human becoming infected but can be seen with some swine influenza viruses as well. Host jumping rarely results in human-to-human transmission.
Swine are, for want of a better phrase, “mixing vessels,” that is they can become infected by both human and avian influenza viruses — sometimes simultaneously. They can also become infected with an avian and a swine virus, or a human and a swine virus at the same time, too. In any of these cases, the new virus produced can have RNA strands of the two viruses that the pig was co-infected with or the new virus can have a mixture of genes from the RNA strands of the two viruses that infected that cell rather than whole strands of RNA from the infecting viruses. In either case, the resulting virus has pandemic potential.
Prior to an epidemic of African Swine Fever, capable of wiping out a whole herd in days, China had over 500 million pigs and approximately 6-7 billion poultry. Very common Chinese “wet markets” pack large numbers of exotic animals, swine, aquatic and poultry birds and humans in close proximity. This environment is ripe for viral infection. The Influenza viruses are going to replicate, sometimes mutate, sometimes host jump and sometimes mix RNA strands or genes. Viruses do not necessarily need to escape from research labs or be bio-manufactured for the next pandemic to occur, they just need the right environmental conditions.
That is the broad perspective. In regard to the G4 strain of H1N1, it does not seem capable of spreading human-to-human. However, the more people that become infected, the more opportunities the virus has to be in a human cellular environment and mutate in a way that enables person-to-person spread.
G4 bears watching and researching, but no alarms need to be sounded… yet.
