Mechanism Of Transmission And Pathosiology Of Influenza
Transmission – The healthy adults influenzavirus shedding (at the time during which a person might be infectious to another person)
this increases sharply at least one-half to one day after infection, peaks on day 2 and persists for an average total duration of 5 days—but can persist as long as 9 days (Klenk et al., 2008). Now one who develops symptoms from an experimental infection (lets take for example, only 67% of the healthy experimentally infected individuals), with symptoms and viral shedding show a similar pattern, but with viral shedding preceding illness by one day (Klenk et al., 2008). Children are much more infectious than adults and shed virus from just before they develop symptoms until two weeks after infection. In immune compromised people, viral shedding can continue for longer than two weeks (Ghedin et al., 2008).
Influenza can be spread in three main ways (Katagiri et al., 2002; Wagner et al., 2008): by a purposefully direct transmission (for example, a situation when an infected individual sneezes mucus directly on the eyes, nose or mouth knowingly or unknowingly on another person); movement of the airborne (when the next individual inhales this aerosols produced by an the person who is infected while coughing or sneezing and even spitting) and also a hand-to-eye or a hand-to-nose, also the hand-to-mouth transmission of contact, either on a contaminated surface or from direct personal contact which could include a hand-shake.
A very relative importance to these three modes of transmission will be referred to unclear, and still get to contribute or even spread of influenza virus (Hilleman, 2002). When its an airborne route, these droplets which are small to be inhaled by people are 0.5 to 5 µm in diameter and inhaling just one droplet might be enough to cause an infection (Wilson and von Itzstein, 2003). Although a single sneeze releases up to 40,000 droplets, most of these droplets are quite large and will quickly settle out of the air (Jakeman et al., 2004). It is yet to be determined the length of time an influenza survives in the airborne droplets when seems it can be influenced by levels of humidity or the UV radiations, with a very low humidity or even the lack of any sun-light in the winter giving it an aiding hand for its survival (Ghedin et al., 2005).
As the influenza virus can persist outside of the body, it can also be transmitted by contaminated surfaces such as banknotes (Bouvier and Palese, 2008), doorknobs, light switches and other household items. The length of time the virus will persist on a surface varies, with the virus surviving for one to two days on hard, non-porous surfaces such as plastic or metal, for about fifteen minutes from dry paper tissues, and only five minutes on skin (Lakadamyali et al., 2003). However, if the virus is present in mucus, this can protect it for longer periods (up to 17 days on banknotes) (Liu et al., 2011). Avian influenza viruses can survive indefinitely when frozen. They are inactivated by heating to 56 °C (133 °F) for a minimum of 60 minutes, as well as by acids (at pH <2) (Kash et al., 2006).
The mechanisms by which influenza infection causes symptoms in humans have been studied intensively. A mechanisms believed to be able to perform as an inhibition for the adreno-corticotropic hormone on (ACTH) which brings a resulting in the lowered cortisol levels. Also knowing the genes that are carried by any particular strain which at the end will help in the predicting of how well it can easily infect a person and how severe this infection will be (that is, predict the strain’s pathophysiology) (Cros and Palese, 2003).
For instance, part of the process that allows influenza viruses to invade cells is the cleavage of the viral hemagglutinin protein by any one of several human proteases (Gooskens et al., 2009). In mild and avirulent viruses, the structure of the hemagglutinin means that it can only be cleaved by proteases found in the throat and lungs, so these viruses cannot infect other tissues. However, in highly virulent strains, such as H5N1, the hemagglutinin can be cleaved by a wide variety of proteases, allowing the virus to spread throughout the body (Hall, 2007).
The viral hemagglutinin protein is responsible for determining both which species a strain can infect and where in the human respiratory tract a strain of influenza will bind (Mitamura and Sugaya, 2006). Any form of strains which can easily transmit in between different people and yet have the hemagglutinin proteins which has the ability to bind the receptors in an upper part of the respiratory tract, this include the nose, the throat and also the mouth. In contrast, the highly lethal H5N1 strain binds to receptors that are mostly found deep in the lungs (Nicholls et al., 2008). A major differences in these area it has caused some infection can be attributed by the part of the reason the H5N1 strain brings about a severe viral pneumonia to an individual’s lungs, but may not easily be transmitted from one person coughing and also sneezing (van Riel et al., 2006; Winther et al., 2008).
One of the most common symptoms of the influenza virus flu such as fever, fatigue, headaches or cold are a few result of a large huge amounts of pro-inflammatory cytokines and also the chemokines (such as interferon or tumor necrosis factor) produced from influenza-infected cells (Kobasaet al., 2007). In contrast give the rhinovirus which is known to cause common cold, the influenza virus causes tissue damage, so also the symptoms are entirely not due to any inflammatory response one gets (Smith et al., 2006).
The massive immune responds with a life-threatening cytokine storm in the system. This also an an effect has always been proposed to be the reason for the unusual lethality of both the H5N1 avian influenza as well as the 1918 pandemic strain (Poole et al., 2006;). Meanwhile, there is a possibility these large amounts in cytokines may be as a result of a massive levels of the viral replication as was produced through these strains, and also the immune response doesn’t on it own contribute to the disease (Beck et al., 2012).