The problem with the flu vaccine isn't mutations in the virus, its because the seasonal genetic reshuffling of antigens is difficult to predict. The genomic structure of the antigens show little to no mutations year to year.
And the reason why the HIV vaccine has proven so hard to develope isn't because of mutations either. It is unique in that B cell stimulation has little effect, and it successfully hijacks the T cells that are needed to direct the immune response. The rapid mutation of HIV has more relevance to the selection of anti-viral treatment.
I'm sorry, but according to numerous sources, Anitgenic drift is an accumulation of variation caused by an accumulation of mutations.
Direct quote from the CDC:
Antigenic Drift
One way influenza viruses change is called “antigenic drift.” These are
small changes (or mutations) in the genes of influenza viruses that can lead to changes in the surface proteins of the virus: HA (hemagglutinin) and NA (neuraminidase).
When antigenic drift occurs, the body’s immune system may not recognize and prevent sickness caused by the newer influenza viruses. As a result, a person becomes susceptible to flu infection again, as antigenic drift has changed the virus enough that a person’s existing antibodies won’t recognize and neutralize the newer influenza viruses.
Antigenic drift is the main reason why people can get the flu more than one time, and
it’s also a primary reason why the flu vaccine composition must be reviewed and updated each year (as needed) to keep up with evolving influenza viruses.
From Bhekisisa Center for Health Journalism:
SARS coronaviruses replicate and mutate relatively slowly when compared to other viruses such HIV, which replicates at a high rate. Because HIV can adapt so quickly, there could be many strains of the virus, and it could potentially become drug-resistant. “[coronaviruses replicate at] a fraction of what you see with HIV,” Preiser explains.
From NPR:
HIV is a complex virus that targets and weakens the human immune system, which is normally responsible for fighting off diseases and infections. It also mutates rapidly, making mistakes as it replicates in the body.
"[This results] in viruses that are not all identical to each other," says Feinberg. "That means in every HIV infected person, there's tremendous genetic diversity." Antibodies created by the immune system to fight off the virus ultimately can't keep up with the mutations and fail to fight off HIV.
A vaccine for HIV faces the same challenge: it must trigger the creation of antibodies that can fight off all the different variations and subtypes of HIV. It also must have a long-lasting effect.
From NIH, though reading the full paragraph gives a fuller explanation (doi:
10.1007/s00018-016-2299-6) :
A similar scenario can be depicted for antiviral immunity.
Viruses showing high mutation rates tend to evade immunity more efficiently. There are numerous examples of cytotoxic T lymphocyte (CTL) and
antibody evasion in HIV-1, HCV, and hepatitis B virus (HBV), three fast-mutating viruses causing chronic infections. In HBV, the most common cause of hepatitis worldwide with nearly 350 million people chronically infected, a series of point mutations have been associated with immune escape and vaccination failure [
7]. In acute viruses, immune escape takes place at the host population level instead of at the intra-host level. In this case, the benefit of escape resides in the ability of the virus to re-infect hosts that have developed protective immunity or infect hosts with that recognize the same antigens. The best-known example is influenza virus, which constantly undergoes antigenic changes and therefore requires yearly vaccine updates. Current efforts focus on developing influenza vaccines that target evolutionarily more conserved, yet sufficiently immunogenic protein domains [
8].
Viral genetic diversity, which is ultimately determined by mutation rates, has therefore a profound effect on the design of antiviral strategies.
