The Potential for H5N1 Avian Flu and Human Flu Virus Hybridization

The question of whether H5N1 avian flu could be combined with a live human flu virus is a matter of significant concern in the field of virology. This hybridization possibility is discussed in the context of the potential for a lethal pandemic strain.

Understanding the Current Situation

The reason we have not yet seen a pandemic spread of H5N1 is that it remains adapted to the alpha23 sialic acid of water-bird gut linings. For efficient human-to-human transmission, the avian viruses need to recognize sialic acids with the alpha26 linkage found in the human upper respiratory tract. The 1918, 1957, and 1968 pandemic viruses suggest they preferred alpha26-linked sialic acids.

The Role of Pigs as Mixing Vessels

Epithelial cells in the pig trachea produce both alpha23 and alpha26 linked sialic acids, which could explain why pigs can be infected by both avian and human influenza virus strains simultaneously. Consequently, pigs can serve as a 'mixing vessel' for the emergence of novel viruses. This scenario is particularly feared because a genetic hybrid virus with the lethal power of, say, H5N1 or H7N9 and the pandemic-spread potential of A/H1N1 2009 is a heightened concern.

The Scenario for Hybridization

Imagine a situation where an individual, either human or pig, is simultaneously infected with a circulating influenza A virus capable of sustained human-to-human transmission, characterized by a low case fatality rate (CFR) - for instance, the 2009 pandemic A[H1N1] pdm09. Simultaneously, this same individual becomes infected with a highly pathogenic avian influenza virus (such as H5N1 or H7N9), which lacks the capability to spread efficiently among humans, but carries a much higher CFR.

The Adaptable Virus Theory

The adaptability of the low-pathogenic virus could, in theory, be transferred to the high-pathogenic virus, enabling it to spread more effectively among humans. Given that many avian influenza viruses are already adapted to pig hosts, this scenario is not far-fetched. It is known from extensive work by Taubenberger and others that relatively few mutations are needed to allow HPAI-H5N1 to attach to alpha26 sialic acid-linked receptors in the human upper respiratory mucosa, rather than the lower respiratory tract where it is similar to water-bird epithelia containing alpha23 sialic acid receptors.

Upper respiratory infection means rapid, pandemic-type spread, which is the ultimate concern. The scenario described above, though complex, is not outside the realms of possibility. Therefore, the imperative remains for continuous surveillance and rigorous public health measures around influenza viruses.

It is crucial to remember the importance of yearly immunization and vigilance in the face of such threats.