Attack of the Swine and Viral Agents

February, 2009 a town in Veracruz Mexico, called La Gloria, is under attack. About sixty percent of the town has a mysterious respiratory malady, and two infants die. March moves along with a few more cases of this strange infection, similar to, but not quite, the common seasonal flu. April comes and while not bringing May flowers, more incidents pop up, moving north into the US and then out into other countries. May arrives and now the WHO has declared a Phase 5 Influenza outbreak, more than forty people have died and over twenty countries around the world have reported confirmed cases. The pigs are attacking.
Or not. While initially named the “Swine Flu,” this new virus is not of any conscious swine nefariousness. Instead it is a new recombination of older influenza, either human, avian and swine, or just a remixing of existing swine influenza, mixed inside a pig carrier.
A virus is an extremely small agent tunable to grow or reproduce by itself. For these reasons, viruses cannot be classified as alive; they need a living host cell to hijack and replicate. Viruses are made of two to three parts; genetic material comprised of either DNA or RNA, a protein shell housing the genetic material, and in some, a protective envelope that helps protect the virus and aids the hijacking of cells. Much like Mr. Smith’s human parasite, viruses must rely on their environment, using it up as they go and then migrating to the next source.
In 1884, Charles Chamberlain invented the Chamberlain filter, a filter that allows bacteria to be strained and kept out of a sample, and for the first time, bacteria could be culled from samples. Eight years later, Dimitri Ivanovski used that filter to study what is now known to be the “Tobacco Mosaic Virus.” Using the filter to remove bacteria from infected tobacco, he showed that, while free from bacteria, the tobacco was still infectious, though he deducted that toxins produced by the bacteria was the cause, blaming the bacteria indirectly. Six years later Martinus Beijerinck, a Dutch microbiologist, repeated the experiment and decided that a new infectious agent, which he called “contagium vivum fluidum,” was the culprit, naming virus and naming it a liquid.
While incorrect in his assumption of the liquid nature of viruses, Beijerinck did finally use the term, virus, and noted that it was separate from bacteria. In 1899, due to dilution tests, viruses were relieved of their toxin state and that they could replicate. Throughout the 1900’s, many advances in virology occurred, including the discovery of vaccines and suppression drugs.
The basic structure of a virus simple, with two to three common parts. A protein shell called a “capsid” encompasses a bit of nucleic acid, either DNA or RNA. In some, a lipid envelope made of the host cell surrounds the protein shell and helps shield the virus. The capsid is constructed by the virus and is the basis for differentiating between different viral morphological types. There are four main morphological types of viruses; helical, icosahedral, enveloped, and complex.
Helical viruses, of which the afore mentioned Tobacco Mosaic virus is, are typically cylindrical, with either a hollow inner section or a cavity inside for holding the genetic material. Their length is proportional to the amount of genetic material contained within. Icosahedral contain most of the animal viruses and are close to spherical in shape. Enveloped viruses are the “wolf in sheep’s clothing” of the viral world, having fashioned an envelope out of the host’s outer or inner membrane. Covered in proteins virally charged, this envelope is usually the primary attacking mechanism of this type of virus and the influenza and HIV viruses are a part of this morphological type. A final type, complex, encompasses many of the other three, but that have a little more, or less. A typical bacteriophage, a bacteria targeting virus, looks much like a lunar lander; a “head” filled with genes, a collar extending down into the sheath which merges with the baseplate, and ending with a set of tail fibers looking like the lander’s legs.
Viruses have two main modes of transmission between hosts in humans; horizontal and vertical. In Horizontal transmission, the virus is transmitted from one host to another via a fluid exchange of some sort, parent to offspring transmission is not considered a part of this. Saliva, blood, sexual fluids are among the culprits for this transmission and HIV and Hepatitis and Influenza are some of the viruses passed on this way. In contrast to Horizontal transmission, Vertical transmission is from parent to offspring. Because the mother is connected to the baby, any of the viruses that she has are able to be passed on due to proximity and are not classified as horizontal, though the same viruses may be transmitted either way.
Once a virus has been transmitted to a new host, or a new site within its current host, it undergoes six basic stages culminating in replication and release. A virus needs to attach itself to a new host cell in order to begin the replication process, where an envelope helps if it has one. Viruses usually bind to cells that are able to replicate them, due to which proteins are capable to be produced. Once attached, the virus must penetrate the cell wall, easier in animals than plants and bacteria, due to the structure of each type of cell. During uncoating, the capsid holding the genetic material is forced to release the nuclear acids into the host cell and replication begins. Replication forces the newly hijacked cell to start manufacturing new proteins and viral genomes and after this assembly period modifications take place. Lysis occurs after this modification and consists of the cell membranes bursting and shooting the viruses out to infect new cells. Enveloped viruses leave via “budding,” essentially bubbling out the membranes to provide enveloped until there is so little membrane left is cannot stay together. After lysis occurs, the process repeats itself.
To combat the viruses, bodies have many tools. The innate immune system is made up of several general mechanisms that protect in the short term, though are easily foiled by the virus’s own defenses. More effective is the adaptive immune system, which produces antibodies that bond to the virus and renders it ineffective at infecting new cells. IgM is the first antibody that begins to work, and starts aggressively, though it only stays for a few weeks, IgG takes a little longer to come into play, but the body maintains them and continues to build them up throughout the rest of its life. By testing each of those antibodies, the state of an infection can be found and whether or not this particular virus has been encountered before. Cell mediated immunity is a secondary measure of defense and also is compromised of several measures.  T cells search for aberrant cells and destroys them, hindering or halting the viruses production capacities. A more extreme measure sees the defense cells destroying the infected cell and many of the neighboring cells in a “fight fire with fire” mentality. Viruses have a myriad of ways to bypass these security measures, so it is a constant struggle between the host and virus.
Due to the number of replications viruses go through, much genetic change is possible. Each cell infected leads to a large number of generic recombinations, which increases dramatically the chances for genetic drift. While the proteins replicated usually aren’t altered of changes, HIV being slightly different here, the changes are often enough to make a resistant strain to existing or used antiviral medicine. These offspring are better suited to live under the current conditions, thought they typically die out to the original strains once the conditions return to normal. This habit can allow for a blasting of the virus after the original, weaker strain has become dominant again, to keep it more fully under control or even eradicated. When the influenza virus undergoes such a mutation, a pandemic can be the result, due to a lack of immunity to this new virus and its spreadability.
Influenza, commonly called the “flu,” is a virus affecting mammals and birds. Common symptoms run the gamut of; chills, fever, coughing, sore throat, muscle pains, cramping, weakness, general discomfort and headaches. Pneumonia, vomiting and nausea are other effects of the virus as well. Typically transmitted via saliva from coughs or sneezes, the flu can also be transmitted by other body fluids and secretions if allowed physical contact. Many of the human pandemics that occurred in the 1900’s were resultant of a strain of the virus normally housed in an animal or bird that was passed to humans, who were left without any immunity to that particular strain. While vaccinations to the virus do exist, they may prove ineffective from year to year due to the high mutability of the virus.
The winter and spring months are the common flu seasons, due to a more receptive and helpful environment. Sneezing expels a large amount of virus laces droplets from a host, who is typically infectious for about ten days after receiving the virus themselves. The lower humidity and lower UV levels in winter and spring help the virus survive during transmission and so a peak in flu outbreaks appear seasonally, both in the northern and southern hemisphere’s, one after the other. Handshakes are also able to transmit the virus from mouth to hand to hand to mouth. The viruses are able to survive being frozen, and this is partly a cause for the alarm that was generated when the Spanish Flu was reengineered, if it were to be reintroduced into the world’s population now, either accidentally or intentionally, almost no one would have any immunity to it and could result in a huge death toll.
Influenza is made up of two proteins and five genera; Influenza A, B, C, Isavirus, and Thogotovirus. The basic differences between Influenza A viruses, which are the most common and mutable in humans, are the number and sequence of proteins hemagglutinin and neuraminidase in the capsid. The other variants of the virus are more stable and therefore less prone to pandemics due to immunities taking longer to become ineffective. The genome is not a singular piece of genetic data, RNA in this case; rather, it has multiple pieces of genes inside it.
1918 saw the rise of the first flu pandemic of the century, popularly and infamously called the Spanish Flu. An unusually virulent strain of the H1N1 strain of Influenza A, the flu had a mortality rate much higher than normal and it came in two waves. Spanish Flu was a misnomer picked up as a result of the times; WWI kept the involved countries closed-mouthed about fatalities and the state of the flu ravaging the world, while Spain, a neutral country, had no censorship and so seemed to be the only country experiencing the effects, as well as the best source of information about it. Research done on the virus has shown that it likely worked by making the immune system of the infected person overwork itself, attacking the otherwise healthy body. This had the curious side effect of doing more damage to healthier young adults, rather than the young children and older adults normally affected the most by influenza. A possible explanation for the decreased mortality rate in young and old was the Russian flu thirty years before having helped to build up the older adults immunities and then further helping the younger children as a byproduct. The Spanish Flu is estimated to have killed as many as 100 million people, around twice as many casualties as the Great War, making it one of the deadliest pandemics of the 20’th century.
H2N2, another subtype of the Influenza A virus, is sometimes called Bird Flu, and mutated into the Asian Flu. A severe pandemic, the virus was originally an Avian flu that combined with a human variant, broke out in 1956 and lasted for two years, while a vaccine developed in 1957 helped contain it. Contrasting with the Spanish flu, which was entirely derived from a species-hopping variant, the Asian flu was a recombination of human and avian influenzas, and later caused a milder pandemic in 1968-1969.
In the late 1960’s, the H2N2 Influenza A virus mutated into a new strain of H3N3 influenza. Titled the Hong-Kong virus because of infecting roughly half a million people there, about 15% of the population. While a product of the Asian flu, it had a fairly low mortality rate, but had an interesting characteristic; it arose in swine, which acted as a kind of breeding ground for human and avian flues. This flu was also the first known outbreak of the H3 type outbreak.
Mid-March, 2009, a town named La Gloria in Veracruz, Mexico had a large percent of its population come down with a strange respiration illness. In April, a new strain of Influenza A H1N1 was clinically identified, and linked to the respiratory illness of La Gloria. By the beginning of May, over two thousand laboratory confirmed cases had been found in over twenty countries worldwide. Found after government officials in the US and Mexico began looking into late season flu cases, the flu has no confirmed start date. On April 29’th the World Health Organization raises its alert level to “Phase 5” of 6, meaning a pandemic is imminent. Previously, the WHO had been reporting on the outbreak and starting a vaccination week in the Americas. By the end of April, governments around the world were beginning to take measures to slow or stop the spread of the virus across borders and into their countries. Around that time, however, scientists began to reach a consensus that the outbreak was much less deadly than originally thought.
The two predominant thoughts on the origins of this new strain vary significantly. At first, it was apparently a reassortment of four strains of Influenza A, a human, avian and two swine strains. Later, it was suggested that all the RNA segments are of swine origin. Swine are viewed as a primary contributor to this outbreak because they are easily able to house both avian and human influenza, acting as a kind of breeding ground for the two of them and as a travel agent for the viruses. Early May, a herd of pigs in Alberta, Canada were quarantines after suspicion of infection. It case was curious due to the fact that the flu would have to have been carried to the pigs by a human, marking the first reverse transmission. Scientists are looking for “Pig 0” the pig that is though to have been a part of the original housing group of the virus.
This outbreak shares many similarities with the other three major pandemics of the last century. Like the Spanish Flu, it is an H1N1 strain, and seems most effective in young adults, though evidence that the virus provokes a cytokine storm is lacking as opposed to the Spanish Flu. Like the Asian Flu, this H1N1 strain is partly believed to have been part of a recombination of avian and human flues. In the same fashion as the Hong Kong Flu, this virus arose out of pigs acting as a breeding ground and then passing it to a human carrier, whether or not human and avian strains were also folded in on the mix.
Despite having originated in swine, and still apparently being able to cross back to them, as seen in the Canadian case, the term “Swine Flu” is no longer being used. This is partly because of the negative impact a decrease in the consumption of pork would have on the already weak global economy and because the safety of cooked pork is not compromised by the virus. Other names such as “Mexican Virus” and “Mexican Flu” have also been shot down for like reasons. Currently, Influenza A H1N1 is the correct verbage according to the WHO, though other organizations may still use other names.
Due to the H5N1 avian flu, the WHO Pandemic Influenza Phase was already set at 3 when the H1N1 virus was first discussed by them on April 25’th. Phase 3 means that while there is a new strain of a flu virus, it is in a relatively isolated circumstance and has not yet gained the ability to cause a pandemic yet. Phase 4 has human-to-human spread of the influenza virus in levels that could cause a community outbreak, but that a pandemic, while possible, isn’t likely, the WHO raised their warning level to Phase 4 April 27’th. Two days later, the WHO raised the level to Phase 5, where human-to-human contact has spread the virus to at least two countries in a WHO region. Phase 6, the highest phase, consists of communities sized outbreaks in a different WHO region, and as of yet has not been achieved.
Initially only in Mexico and the US, the H1N1 virus has begun to spread to other countries as well. March had La Gloria, Veracruz, Mexico attacked by a widespread respiratory illness, and the earliest case in the US of the virus. April 24’th, the WHO issued its first disease report, and planned a vaccination week the day after. On April 26’th, Canada reported its first four cases of the virus. The next day, Spain confirmed its first case, and the first European transmission of the virus, Scotland confirmed two additional cases as well that day. Israel and New Zealand report cases April 28’th and Germany, and Austria likewise the 29’th. April 30’th has the Netherlands, Switzerland,  and Ireland showing cases of infection. May 1’st sees Hong Kong quarantine three hundred people in a hotel due to seven cases, Denmark and France both confirm cases. Italy, South Korea and Costa Rica, which was the first Central American country yet, confirm cases on May 2’nd. Columbia becomes the first South American country to confirm and Portugal also confirms on May 3’rd, followed by El Salvador the next day.  Guatemala confirms its first case on the 5’th while Poland confirms on the 6’th.
While a previously unknown and likely a new strain, the new H1N1 virus has not shown itself to be highly virulent as of yet. Several of its protein strands are similar to those that cause only mild symptoms in other strains of the influenza virus. While most of the deaths have occurred in the young adult category, the only deaths that have occurred yet have been in the US and Mexico and the mortality has not followed out of those two countries. While the H1N1 virus is showing to be resistant to the seasonal Influenza type A H1N1 vaccine, amantadine and rimantadine, it is showing to be sensitive to oseltamivir and zanamivir. Soap and water or alcohol based cleansers help stymie the progress and transmission of the virus, as with other strains of the virus.
Symptoms of the H1N1 virus include the normal flu symptoms. Runny or stuffy nose, and headache are common maladies. A specific cough is also characteristic of this flu, and diarrhea is in addition to the normal symptoms. Because most of the deaths have occurred in the developing nation of Mexico, the possibility that the virus targets more effectively in poorer conditions is real, as evidenced in the La Gloria outbreak.
Other widespread viruses are the HIV (human immunodeficiency virus) virus and the five hepatotropic viruses. In contrast to the influenza viruses, HIV is a primate centric virus in that those two strains that have infected humans both came from primates, HIV-1 from the common Chimpanzee and HIV-2 from old-world monkey Sooty Mangabey. Both strains evolved from SIV (simian immunodeficiency virus) though from different base species as noted above. The owl monkey is interesting in that it has a resistance to HIV-1 due to a fused gene.
Transmission of the HIV virus is primarily done in three ways. Sexual transmission makes up the majority of HIV infections when unprotected sex is practiced. Blood related practices also provide a high level of HIV infections, especially in third world countries. Mother to child transmissions are also possible, in three particular periods. “In utero” or during pregnancy, “intrapartum” which is at childbirth, and during breastfeeding are all ways to spread the virus, though with the correct habits and medication, the breastfeeding risk drops substantially. HIV-2 is much less likely to contract via the mother to child rout than HIV-1.
HIV is an enveloped virus and both variants attack the same types of cells. HIV-1 will bind to any RNA without preference, whereas HIV-2 is more selective. Because HIV-2 is more selective, it takes longer to replicate itself and longer for AIDS to settle in, it also takes more time to mutate. Due to the extremely fast replication cycle, HIV has an high degree of genetic variability and there are three main groups of HIV-1, each with its own subgroups. HIV-2 more closely resembles SIV and has fewer variances.
Because HIV attacks T cells, depletion results in AIDS. The loss of T cells correspondingly results in a lack of the ability to combat any further infection or illnesses that come along, due to a compromised immune system. As a result, the host is at risk of dieing over almost any malady that attacks and must go on a regiment of medication and antivirals to be able to cope with the environment around them.
Viral hepatitis is caused by another common group of viruses. While Hepatitis A, B, C, D, E and F all share a name and cause liver inflammation, they are unrelated.  The  hepatitis A and E viruses transmit in an Enteric mode while the other three transmit in a Parenteral mode.
HAV transmits via the fecal-oral route, usually either by eating contaminated food or anal-oral sex. Roughly 15% of the infected may experience symptoms out for a year past the initial diagnostic, while the remainder usually recover within about two months. HBV develops chronically in about 15% of adults who are unable to eliminate the virus after infection. HBV is transmitted via blood, tattoos, sexually, and breastfeeding, with roughly half the sources of the infection being unknown. HCV is the most common bloodborn infection in the US and transmitted via blood and usually leads to chronic hepatitis.
Symptoms of viral hepatitis vary. Hepatitis A can be mistaken for the flu, and include abdominal pain, diarrhea, loss of appetite, depression, jaundice, weight loss and itching. Hepatitis B contributes to dark urine and general sickness, as well as liver disease. Chronic hepatitis C has a risk of liver inflammation and scarring, bruising and bleeding tendencies and hepatic encephalopathy, a neuropsychiatic abnormality in the setting of the liver. HDV needs HBV to propagate, so it is considered a subviral satellite, and infection exacerbates that of the HBV.
Viral diseases and maladies come in many shapes and forms. Because of the replication processes that they go to, viruses have a high degree of mutability and are able to undergo rapid changes in a relatively short time. The resultant generations can be totally new viruses and thus either more or less effective at infiltration of cells and further replication. Indeed, if a virus becomes so adept as infiltrating, replicating and expanding, it may outgrow its environment too quickly and loose the chance to further grow and develop. Likewise, a mutation may hamper the virus from replicating quickly enough and will then die out. So remember; it’s not the pigs who are attacking, it’s the viruses.

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