Global migration of influenza viruses
Influenza A virus is able to persistently re-infect human populations by continually evading host immunity through the continuous and rapid evolution of surface antigens. This process is known as antigenic drift. Influenza virus epidemics affect temperate latitudes of the world each winter, from November to March in the northern hemisphere and from May to September in the southern hemisphere. In the United States alone, these influenza epidemics are associated with an annual average of 36,000 human deaths and 226,000 hospitalizations. Globally, the virus is associated with as many as half a million annual deaths. While rapid antigenic change is characteristic of influenza, recent studies have failed to detect antigenic drift over a single epidemic season, suggesting that important evolutionary processes may occur during non-epidemic periods, either locally or perhaps elsewhere. However, surveillance during non-epidemic periods is not conducted routinely by the network of World Health Organization influenza reference centers and, consequently, little is known about how and where the virus persists in the human population in between winter epidemics at low levels. A key question is therefore whether the virus remains locally within its host population in between epidemics, perhaps persisting within hosts in a latent state, or whether the virus migrates to other reservoirs, such as the tropics, and is later reintroduced.
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Although influenza virus has long been regarded a “cold-weather” pathogen due to its marked winter epidemics in temperate zones, recent studies show that tropical regions experience significant year-round influenza virus activity. In theory, such a “tropical belt” could serve as a year-round reservoir that harbors endemic populations of influenza virus that seasonally reintroduce viral isolates into temperate zones to trigger new epidemics. Whereas population crashes at the end of seasonal epidemics create severe evolutionary bottlenecks that limit genetic diversity, tropical zones may function as permanent mixing pools for viruses from around the world. Historically, Southeast Asia has been considered a potential epicenter for emergence of pandemic viruses due to the proximity with which humans live with their domestic animals. However, abundant data from these regions is currently unavailable, so the origins of influenza pandemics and epidemics remain unclear.
Given the ease and speed with which the influenza virus is thought to spread between humans, it is generally accepted that global chains of direct person-to-person transmission are sufficient to maintain influenza virus in the human population. However, a complete understanding of how the influenza virus transmits between humans is lacking, and whether human-to-human spread alone accounts for the seasonal emergence of epidemics has been questioned. The simultaneous appearance of influenza outbreaks separated by large distances, as well as sporadic influenza cases during summer months, suggests that the virus may instead already be “seeded” and somehow reactivated by environmental stimuli. The alternating pattern of northern and southern hemisphere epidemics could, in principle, also result from opposite climatic forces independently reactivating viral activity in these two hemispheres at alternating six-month intervals. Hence instead of continually migrating across the equator, separate virus populations could persist locally in an asymptomatic latent state over the summer months until climatic stimuli sufficiently increase host susceptibility and/or viral transmissibility to induce another epidemic. However, hypotheses of how climatic change may directly or indirectly influence viral activity and/or host susceptibility remain largely untested.
Some theories for influenza seasonality produce testable hypotheses. On one hand, if influenza virus persists locally over the summer in a latent state, then isolates sampled over multiple seasons from a single locality would cluster together on a phylogenetic tree, separate from isolates from other geographic regions. Alternatively, if the virus did not evolve locally between epidemic seasons, but rather traveled globally between epidemics, then the resulting phylogeny would show extensive intermixing of isolates from different localities. To determine whether influenza virus migrates between the northern and southern hemispheres during non-epidemic summer months or remains localized, a recent paper in PLoS Pathogens reports on an extensive phylogenetic analysis of 399 influenza A viruses sampled from New Zealand from 2000 to 2005, 88 virus sequences from Australia from 1999 to 2005, and a carefully selected sample of 52 isolates which are representative of the types present in a larger sample of 413 viruses in the USA from 1998 and 2005 (Phylogenetic Analysis Reveals the Global Migration of Seasonal Influenza A Viruses. PLoS Pathog 3(9): e131).
The results show that even in areas as relatively geographically isolated as New Zealand’s South Island and in Western Australia, global virus migration contributes significantly to the seasonal emergence of influenza A epidemics, and that this migration has no clear directional pattern. These observations run counter to suggestions that local epidemics are triggered by the climate-driven reactivation of influenza viruses that remain latent within hosts between seasons or transmit at low efficiency between seasons. However, a complete understanding of the seasonal movements of influenza A virus will require greatly expanded global surveillance, particularly of tropical regions where the virus circulates year-round, and during non-epidemic periods in temperate climate areas.
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