Estimates of the Transmissibility of the 1968 (Hong Kong) Influenza Pandemic: Evidence of Increased Transmissibility Between Successive Waves

Abstract

The transmissibility of the strain of influenza virus which caused the 1968 influenza pandemic is poorly understood. Increases in outbreak size between the first and second waves suggest that it may even have increased between successive waves. The authors estimated basic and effective reproduction numbers for both waves of the 1968 influenza pandemic. Epidemic curves and overall attack rates for the 1968 pandemic, based on clinical and serologic data, were retrieved from published literature. The basic and effective reproduction numbers were estimated from 46 and 17 data sets for the first and second waves, respectively, based on the growth rate and/or final size of the epidemic. Estimates of the basic reproduction number (R0) were in the range of 1.06–2.06 for the first wave and, assuming cross-protection, 1.21–3.58 in the second. Within each wave, there was little geographic variation in transmissibility. In the 10 settings for which data were available for both waves, R0 was estimated to be higher during the second wave than during the first. This might partly explain the larger outbreaks in the second wave as compared with the first. This potential for change in viral behavior may have consequences for future pandemic mitigation strategies.

Increased transmissibility explains the third wave of infection by the 2009 H1N1 pandemic virus in England

“…S42), which may have substantially affected the ability of the virus to transmit compared with the first (MayAugust 2009) or the second wave (September-December 2009), both of which occurred largely outside the usual period for influenza transmission in northern hemisphere temperate countries. Secondly, signs of adaptation of H1N1pdm09 virus to the human host and the rise of distinct clusters were observed in the United Kingdom (4,5) and in Taiwan (16) Analyses suggest that the basic reproduction number (and hence the underlying virus transmissibility) increased between successive waves of the 1968-1969 pandemic (18), although in that case, there is evidence that antigenic evolution occurred (19,20). We found that although the effective reproduction number R e declined from wave 1 to wave 2 of the 2009 pandemic in England, underlying virus transmissibility may nevertheless have increased over that time.…”

Linking Influenza Virus Tissue Tropism to Population-Level Reproductive Fitness

“…Pathogenicity (P) was used to estimate the transmission rate (β h ) because lesions and clinical signs associated with influenza may on the one hand impede viral transmission (e.g., through damage to the muco-ciliary escalator, mechanical obstruction of the airways or both) and on the other hand impair infected individuals thereby reducing contacts between infected and non-infected individuals. The maximum value of β h was fixed so that R 0 reached a maximum between 2.5 and 3.5, in accordance with R 0 estimates of pandemic influenza viruses in the human population [58], [59]. The mortality rate (α h ) was set as a positive function of pathogenicity (P).…”

H1N1 Influenza Pandemic of 2009 Compared With Other Influenza Pandemics: Epidemiology, Diagnosis, Management, Pulmonary Complications, and Outcomes

“…The virus spread from China in July, but the explosive outbreak was delayed by 6 months. The second wave was more severe and the virus was more transmissible than it had been in the first wave [9].…”

“…The 1957 and 1968 pandemics, which resulted from reassortment between circulating descendants of the 1918 human virus and circulating avian influenza strains, were not as deadly as the 1918 pandemic [9].…”