Why is Hep A clinically silent in the majority of young children?

[Bleepbloopblop]

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[mk04447]

The outcome of hepatitis A infection varies from inapparent or subclinical hepatitis (neither symptoms nor jaundice) that is usually observed in children, to anicteric hepatitis (symptoms without jaundice) or icteric hepatitis that occur primarily in adults leading occasionally to fulminant hepatitis and death, especially in patients older than 50 years (Table 1). More than 70% of adult clinical cases are jaundiced. The molecular mechanisms and immune responses responsible for these outcomes are being addressed and can be summarized as follows. Clinical studies in humans and chimpanzees have shown intrahepatic disruption of the two major cellular interferon‐activating pathways by HAV 3C protease precursors that are formed during the initial stages of genome translation and polyprotein processing.1, 10, 11 Thus, HAV may have evolved strategies to evade protective host innate immune responses typically induced by double‐stranded RNA replicating forms and intermediates, thereby facilitating HAV replication during the clinically silent early stages of the infection.8Subsequently, hepatocellular injury and viral clearance ensue, but the mechanisms responsible for these events have only partially been characterized. A direct cytopathic effect can be excluded due to the presence of large quantities of virus in the liver and stools prior to the onset of hepatitis, as well as the fact that wild‐type HAV is not cytopathic in cell culture, nor does it lead to alterations in cellular metabolism.

Don't ask where I found this, couldn't find it again. I read this to be saying, immature immunity and injury free/healthy liver is the answer.

 

[Bleepbloopblop]

The outcome of hepatitis A infection varies from inapparent or subclinical hepatitis (neither symptoms nor jaundice) that is usually observed in children, to anicteric hepatitis (symptoms without jaundice) or icteric hepatitis that occur primarily in adults leading occasionally to fulminant hepatitis and death, especially in patients older than 50 years (Table 1). More than 70% of adult clinical cases are jaundiced. The molecular mechanisms and immune responses responsible for these outcomes are being addressed and can be summarized as follows. Clinical studies in humans and chimpanzees have shown intrahepatic disruption of the two major cellular interferon‐activating pathways by HAV 3C protease precursors that are formed during the initial stages of genome translation and polyprotein processing.1, 10, 11 Thus, HAV may have evolved strategies to evade protective host innate immune responses typically induced by double‐stranded RNA replicating forms and intermediates, thereby facilitating HAV replication during the clinically silent early stages of the infection.8Subsequently, hepatocellular injury and viral clearance ensue, but the mechanisms responsible for these events have only partially been characterized. A direct cytopathic effect can be excluded due to the presence of large quantities of virus in the liver and stools prior to the onset of hepatitis, as well as the fact that wild‐type HAV is not cytopathic in cell culture, nor does it lead to alterations in cellular metabolism.

Don't ask where I found this, couldn't find it again. I read this to be saying, immature immunity and injury free/healthy liver is the answer.

Thank you !

 

[mistafab]

To dumb this excellent explanation down... I was taught that essentially the “damage” from this infection is primarily (like most things) caused by our immune response to the infection. So children with a less robust immune system are more likely to have a subclinical reaction to it than the full response.

Is this ‘also’ correct?

The outcome of hepatitis A infection varies from inapparent or subclinical hepatitis (neither symptoms nor jaundice) that is usually observed in children, to anicteric hepatitis (symptoms without jaundice) or icteric hepatitis that occur primarily in adults leading occasionally to fulminant hepatitis and death, especially in patients older than 50 years (Table 1). More than 70% of adult clinical cases are jaundiced. The molecular mechanisms and immune responses responsible for these outcomes are being addressed and can be summarized as follows. Clinical studies in humans and chimpanzees have shown intrahepatic disruption of the two major cellular interferon‐activating pathways by HAV 3C protease precursors that are formed during the initial stages of genome translation and polyprotein processing.1, 10, 11 Thus, HAV may have evolved strategies to evade protective host innate immune responses typically induced by double‐stranded RNA replicating forms and intermediates, thereby facilitating HAV replication during the clinically silent early stages of the infection.8Subsequently, hepatocellular injury and viral clearance ensue, but the mechanisms responsible for these events have only partially been characterized. A direct cytopathic effect can be excluded due to the presence of large quantities of virus in the liver and stools prior to the onset of hepatitis, as well as the fact that wild‐type HAV is not cytopathic in cell culture, nor does it lead to alterations in cellular metabolism.

Don't ask where I found this, couldn't find it again. I read this to be saying, immature immunity and injury free/healthy liver is the answer.

 

[mk04447]

To dumb this excellent explanation down... I was taught that essentially the “damage” from this infection is primarily (like most things) caused by our immune response to the infection. So children with a less robust immune system are more likely to have a subclinical reaction to it than the full response.

Is this ‘also’ correct?

Essentially click the answer choice that involves immature immunity. However, it doesn't sound like the immune response is damaging, has to do with HAV evasion and replication that cannot be capitalized on in the younger host. But, I'm reading the same blurb you are, that's just my interpretation.