H7N9 snapdate: age with time

Click on image to enlarge.
Age groups selected to convey clearest trends
without too many lines.

A quick look at some age bands followed each week during the course of both waves of the avian influenza A( H7N9) virus outbreak.

The interesting line to watch is that of the youngest age group (0-19-years) which has lifted to comprise 50% of cases in the week beginning 27-Jan. Also, the proportion of cases in the oldest age group (70->90-years) has dropped down in the past 2 weeks. 

There have been a rash of children in recent announcements; 8 of the last 45 cases have been <10-years of age. For a virus with a median case age sitting at 58-years, this is quite a departure. 

Is this due to an increase in familial clusters? Does it herald a shift in the way the virus is spreading? Intrafamilial transmission may provide a hint at increasing transmission efficiency. It might also be a sign of increased testing augmenting clinical observation of close contacts of ill family members. 

It bears watching closely whatever is happening because its different for some reason. Also worth watching is the downward creeping age. In 2013 the median age was 55.5-years and in 2014 it is 53.5-years. Among the past 45 cases it sits at 52.0-years. 

Tonight we have 310 H7N9 cases ( a third in Guangxi province bordering Vietnam has just popped up while I was writing this paragraph and I've altered the numbers above), with at least 50 deaths (that can be accounted for using public data).

Influenza A(H7N9) virus case accumulation for 2013...

Click on image to enlarge.

Sure a full 12-months of H7N9 in humans hasn't passed yet, but 2013 is coming to a close. 

I have 148 H7N9 cases worldwide including deaths and the asymptomatic boy from Beijing who seems to still be off the official tallies for some reason. WHO have not had an official tally of fatal cases in their recent 2 disease outbreak news posts, the last with a tally was 6-Nov in which 45 deaths were recorded with 6 cases remaining in hospital and 88 having been discharged. Hong Kong's Centre for Health Protection (CHP) maintains a running tally of mainland China cases With the recent death of a Hong Kong man the tally of fatal cases rest around 46 (PFC of 31.1%).

I've just changed my spreadsheet to a weekly format from the daily version and the first chart it reveals is shown above. 

This includes the lay of the land for all H7N9 cases from the beginning of the outbreak, 11-Feb (date of pneumonia for son of index case), through to 29-Dec. Date data employ dates of reporting if no date of illness onset could be found.

We can see from this 47-week inclusive dataset that the principle period of activity was in late March to late April. Whether that will also be the case in the new year is anyone's guess really.

What we can say from the vast amount of influenza virus research data in the scientific literature, is that each and every new combination of 8 gene segments that comprise a distinct influenza A virus seem capable of their own distinct "personality".

Ways in which seasonal and pandemic influenza infections differ

In commenting on another article in the American Journal of Pathology but Gao et al, Kevin Hartshorn nicely summarizes some of the possible reasons why a pandemic influenza kills otherwise healthy young adults more often than a seasonal influenza does. 

The answer is as complex as the milieu of interactions between viral proteins and nucleic acids and our innate and adaptive immune systems, our health, genetic factors, environmental factors and our prior exposure to different influenza viruses - and that's pretty complex!

Hartshorn categorizes the differences between seasonal and emerging influenza impact in young adults using 3 sections:

1. Differences in their ability to cause disease (pathogenicity).
• pandemic influenza generally kill more young adults whereas seasonal influenza kills mostly the elderly and the young
• This is also apparent in ferret animal models
• The viral haemagglutin (HA) protein is key to pathogenesis, playing a central role in pathology due to immune responses and inflammation whereas increases in viral replication are due to the viral replication complex (including PB1, PB2 and PA). Glycosylation of HA is a key pathogenicity determinant because a lack of apical glycosylation allows viral escape from a major non-specific defence; the action of surfacant protein D.
2. Differences in the way the infected host responds to them.
• Pregnant mice and humans show increased severity of disease. This may relate to a reduced innate immune response to pandemic influenza. Bypassing innate immunity may also allow the virus to bypass a key regulatory process, leading to a more over-reactive inflammation.
3. Differences in past history of influenza virus exposures
• Possibly, even with a strong immune cell response, the absence of any prior exposure to a related influenza results in the absence of any cross-protective neutralizing antibodies - the type that can moderate disease - in younger adults compared to older adults. The elderly may have such antibodies from exposures to other H1N1 strains between 1918 and 1957.