The ONLY medical story anyone is discussing currently is influenza, so let’s review quickly. Influenza is an RNA virus(genetic material RNA not DNA) that is identified by 2 “antigens”–outer coat proteins –called hemagglutinin (H) and neuraminidase (N). There are a dozen+ variations of both H and N found on different “strains” of the virus which mutate via 2 pathways: “antigenic drift”–small changes of only a few molecules on the protein render it unfamiliar to the immune system’s defenses; and “antigenic shift”–a more dramatic change in the chemical makeup of H, N, or both. When that happens we may get pandemics–more extensive, serious infections. This happens periodically–1959, ’68, 2009, and the granddaddy of all flu seasons, 1919, when, worldwide, millions died. That event remains the worst flu pandemic in modern history –still the stuff of public health workers’ nightmares.
Given the large number of different H’s and N’s, there are literally hundreds of possible flu combinations. Practically, however, we really only have a few that cause most problems–H1N1, H2N2, H3N2, H5N1, H1N2, and a few others. These are the strains that infect humans, pigs, and domestic poultry(chickens, ducks). It is the interplay of influenza infecting these various host species that enables these buggers to change so subtly but effectively to make us sick every year.
Vaccine is produced by growing virus in egg culture in “the off season” and then noting how the H’s and N’s change, predicting and producing shots based on those observations. However, the virus mutates at variable and unpredictable rates, so it can still change at least a bit after vaccine is manufactured. Most of these “escape mutations” are meaningless as they usually render the virus LESS transmissible. But when it goes the other way the vaccine becomes less effective as it may “miss the target.” While that occurrence is relatively infrequent, given the speed and frequency that flu mutates it still is not rare–including this year, when estimates for vaccine effectiveness are only 10-30%.
We hear a lot about tamiflu (oseltamivir), which blocks production of N. Without N the virus cannot break out of infected cells to attack other cells, curtailing infection. The idea is to start early enough to block virus spread across your body and shorten illness duration. Later in the course, “virus load” is much higher–treating after 48 hours is literally “shutting the barn door after the horse escapes.”
The evidence for tamiflu is somewhat mixed. Lancet reported strong effect, but that was mostly on mortality in seriously ill, hospitalized people with flu. The Cochrane Collaboration study found more limited benefit–<24 hrs symptom relief. Side effects were infrequent–<5% GI (diarrhea, nausea, pain) and <1% psychiatric (confusion or lethargy.) More severe psychiatric problems were only anecdotal.
My own experience is that tamiflu is mild and safe, but also of only limited benefit. So I feel it’s useful–especially if started <48 hours–but no miracle and certainly not essential. Best to focus on fever control, rest, and lots of fluids. So give me a call to discuss.
Thanks for following.