hepatitis A outbreak has raised eyebrows in June, 2013:
At least 87 people are now sick in eight states and 36 have been hospitalized with acute hepatitis A infections tied to a contaminated frozen berry and fruit mix sold at Costco and Harris Teeter stores.In this article, we will examine a different perspective of hepatitis A on human's health: It could be beneficial unless you have the long form of TIM-1 in your gene and Hepatitis A infection have caused you liver failure (see below).
What's Hepatitis A?
Hepatitis A is an acute infectious disease of the liver caused by the hepatitis A virus (HAV). Hepatitis A is spread when human feces contaminates food or when an infected food handler prepares food without appropriate hand hygiene. The viral liver disease can cause mild to severe illness lasting a few weeks to several months.
In a research, scientists have found that there exists a population at higher risk for HAV-induced liver failure, in contrast to the asymptomatic or mild disease experienced by the majority of patients. Patients having one or two copies of the long form of TIM1, a member of the TIM (T cell, immunoglobulin, and mucin domain) gene family, was associated with a greater risk of developing severe HAV-induced liver failure, while having the short form was associated with protection against severe hepatitis.
Symptoms of HAV infection can include:
Hepatitis A and Allergic Diseases
The orofecal route (or alternatively the oral–fecal route or fecal-oral route) is a route of transmission of a disease, when pathogens in fecal particles pass from one host and introduced into the oral cavity of another host. Hepatitis A traveled the orofecal route: Widespread infection meant that stool regularly ended up in food and water. And, hepatitis A infection might simply be a marker for other orofecal infections in general.
An epidemiologist named Paolo Matricardi looked at allergic disease in more than 1600 Italian air force cadets. Those infected with hepatitis A, he found, had half the risk of allergy of those who'd never encountered the virus.
The same conclusion was also drawn from the data collected during the Third National Health and Nutritional Examination Survey, or NHANES, in US. The researcher have found that:
The study also looked at other parasites that are infected via orofecal route:
Interestingly, scientists have found that: The protective effect for allergies was additive. Infection with one bug lowered the chances of allergy by nearly one-third. Infection with two or more lessened the odds by half again. In all, there was a nearly threefold difference in allergy risk between cadets exposed to more than one of these parasites compared with those exposed none.
By comparison, diseases which were infected via airborne route:
Figure 1. The immunopathology of hepatitis A and its relationship to allergic disease.
Later scientists have proposed that allergic disease didn't result from excess exposure to allergens, but from limited exposure to microbes (for example, the ones affect us via orofecal route). Scientists used the seesaw model of the immune system to explain the phenomenon[7, 10,11].
The immune system had two mutually exclusively responses:
This HAV-induced protection against allergic diseases, particularly allergic asthma, has been known for some time. It was first reported that the frequency of multiple sclerosis and type 1 diabetes, two autoimmune diseases, was negatively correlated with anti-HAV seropositivity, used as a marker of poor hygiene.
It was thereafter established in a case-control study that patients with anti-HAV antibodies developed reduced frequency of allergic asthma when compared with HAV antibody–negative subjects . Furthermore, it was shown that among anti-HAV antibody carriers, individuals expressing the long form of TIM-1 were protected from allergic asthma .
How can one reconcile these observations? An interesting possibility is that the long form of TIM-1 is associated with a “strong” response to HAV, which will contribute first to severity of hepatitis and secondly to protection against allergy (Figure 1). If this were the case, it would suggest that it is not only the existence of an anti-HAV response that affords protection, but rather its intensity, the underlying molecular mechanisms of which remain to be defined. This explanation would fit with some of the mechanisms proposed to explain the hygiene hypothesis, notably antigenic competition, which suggests that strong anti-infectious immune responses compete with responses against weak antigens such as allergens and autoantigens.