Yeah strain is a poorly defined term, some researchers have chosen to use it to describe lineages of SARS-CoV-2 with a single amino acid difference. I suppose you could use that definition if that amino acid change has a significant effect on virus physiology e.g. if it alters its transmissibility or virulence. There is a suggestion that one such amino acid change in the spike protein (D614G, or the "G-variant", which sounds like something out of resident evil) has increased transmissibility. As far as I know (from asking someone working on covid genomics at work) this variant does account for 97% of cases, but the jury is still out as to whether that is because of increased transmissibility or not (see short
paper).
As for whether the diversity of "strains" can affect the efficacy of a vaccine, it definitely could but the extent to which it could is not clear yet. From what I understand, the mutation frequency of SAR-CoV-2 hasn't been fully characterised but seems to be in line with other coronaviruses, less than influenza, and significantly less than HIV (if I remember correctly there is as much genetic variation of HIV in one patient than there is of influenza around the world). The efficacy of a vaccine candidate is dependent on two things; 1) how robust the immune response is and how long the resulting immune memory lasts 2) whether the virus does anything to evade the resulting immune response, such as pick up mutations (antigenic drift).
1) We don't yet know how long the immune memory to SARS-CoV-2 infection will last, but we can say that SARS-CoV-2 specific antibodies last at least 3 months, as that is how long we've been able to measure so far. After that you can try and draw conclusions from other coronaviruses, for the common cold coronaviruses it is often stated that the immune memory lasts about a year (although I heard one virologist say that this assumption is based entirely on one paper, that also showed people who are reinfected don't develop symptoms
link to podcast). In contrast, specific antibodies to SARS-CoV-1 last 2-3 years, and memory T-cells have been found 17-years after recovery from SARS
Paper about T-cell responses in SARS-1&2 . There is an idea that the degree of immune memory is dictated to some extent by the severity of infection, which seems intuitive in this situation given the severity of SARS infection. So it is tricky to draw any conclusions from comparing to other coronaviruses, as there is a large variation in the severity of COVID-19 cases. As for a vaccine, you would hope that some of them will generate a robust immune response with lasting memory, which seems might be the case from phase 2 data (although I'm not sure how/if they can comment on memory this early?).
2) It is possible that the selective pressure of a vaccine could select for mutations that confer vaccine resistance, at which point the vaccine would need to be redesigned like for the flu. This is one of the arguments for co-ordinated mass vaccination, as less circulating virus reduces the rate at which new variants will arise. The reduced mutation frequency compared to influenza might help prolong the lifetime of a vaccine. Are there existing variants that could evade the vaccine? I'm not sure about this, I guess the people developing vaccines will have a close eye on any spike mutations that crop up.
I am pretty positive for an effective vaccine, based on the info above. It might not be one of the first wave, but there are a lot in development. Even a 50% effective vaccine could help us restore a large degree of normality.
Disclaimer: I work on bacteria not viruses and am not an expert in virology or immunology.