The impact of this pandemic was not limited to 1918–1919. All influenza A pandemics since that time, and indeed almost all cases of influenza A worldwide (excepting human infections from avian viruses such as H5N1 and H7N7), have been caused by descendants of the 1918 virus, including "drifted" H1N1 viruses and reassorted H2N2 and H3N2 viruses. The latter are composed of key genes from the 1918 virus, updated by subsequently incorporated avian influenza genes that code for novel surface proteins, making the 1918 virus indeed the "mother" of all pandemics. [Until Covid-19]
With the appearance of a new H2N2 pandemic strain in 1957 ("Asian flu"), the direct H1N1 viral descendants of the 1918 pandemic strain disappeared from human circulation entirely, although the related lineage persisted enzootically in pigs. But in 1977, human H1N1 viruses suddenly "reemerged" from a laboratory freezer (9). They continue to circulate endemically and epidemically.
It citest a somewhat obscure paper for that 1977 event. I've actually read the 1978 paper (now) but it leaves me somewhat more confused. It says this about the putative origins of the re-emergence:
The close similarity in both the HA and NA of A/USSR/77-like strains with a 1950 reference virus raises many questions as to the origin of the current H1N1 genes. Because antigenic drift has been observed in animal influenza viruses of several subgroups that have been isolated over a period of years ((16) and R. G. Webster, personal communication), it has been considered unlikely that the H1N1 virus could have been maintained in an animal reservoir for a quarter century without undergoing detectable mutation. Therefore, some have speculated that the epidemic may have resulted from a man-made event. However, it must be noted that the Hav1 antigen of fowl plague virus and the Heq1 antigen of equine influenza virus, which appear to be distantly related (17), have been stable for many years in viruses isolated from birds and horses, respectively ((18) and unpublished results). Chemical studies of all genes in the A/USSR/77-like isolates are, therefore, being done to further examine the question of the origin of this virus (personal communication from Drs. W. Bean, P. Palese, and C. Scholtissek).
The contrast between the homogeneity of antigenic specificity of the HA in 1977-1978 isolates of H1N1 influenza and the antigenic heterogeneity of the HA in viruses in the 1950-1951 epidemics does suggest, however, that current H1N1 viruses arose from a single source. This is also supported by the observed uniformity of avidity of the HAS in 1977-1978 isolates, since avidity also is believed to be a genetic characteristic of influenza viruses (7). Variant viruses that co-circulated in 1950-1951 presumably arose by mutation and evolution from strains widely seeded in the human population during the preceding years, as has also been observed more recently for H3N2 influenza A strains (19).
Note added in proof: Preliminary results of analysis of about 500 H1N1 strains of influenza A virus isolated from about February to May 1978 suggest that approximately 5% of the viruses exhibit minor antigenic drift away from the A/USSR/77 reference strain, and that several distinguishable groups of such variants may be detected. None of the variants, however, appear to resemble A/England/1/51 or other H1N1 strains isolated in the period of former prevalence of such viruses. Presumably, therefore, the newer variants represent examples of mutants of the A/USSR/77-like virus which have appeared following its spread through large segments of the human population.
While this paper entertains the idea of a laboratory release, it doesn't quite seem to fully back it up. So, has any additional research been done since then on the matter, that can (better) explain what Taubenberger and Morens [seem to] claim about the 1977 event?