Lack of antibody response to Guillain–Barré syndrome-related gangliosides in mice and men after novel flu vaccination

During a mass vaccination campaign in the USA in 1976, there was a statistically significant increased risk of developing Guillain–Barre syndrome (GBS) following receipt of the A/NJ/1976/H1N1 ‘swine flu’ vaccine.1 Because the currently circulating pandemic A (H1N1) flu virus is partially of swine origin, there has been concern about a similar association of GBS with the novel flu A (H1N1) vaccine. Preliminary analysis showed an elevated, statistically significant association between 2009 H1N1 vaccination and GBS.2 If confirmed, the increased risk of GBS associated with 2009 H1N1 vaccine of 0.8 cases per 1 million vaccinations would be comparable with the risk described previously for some trivalent seasonal flu vaccine formulations. GBS is divided into two major subtypes, acute inflammatory demyelinating polyradiculoneuropathy (AIDP) and acute motor axonal neuropathy (AMAN).3 AMAN, but not AIDP, is significantly associated with IgG antibodies against GM1, GM1b, GD1a, GalNAc-GD1a and GD1b. It is not known if the 1976 flu vaccine was associated with AIDP or AMAN. A recent report, however, demonstrated that the 1976 swine flu vaccines, seasonal flu vaccines from 1991–1992 and 2004–2005, and recombinant haemagglutinin proteins derived from high pathogenic avian H5N1 viruses A/HK/156/97 and A/Vietnam/1203/04 induced IgM and IgG anti-GM1 antibodies in mice.4 Here, we report our assessment of the pandemic 2009 A (H1N1) and H5N1 vaccines' ability to induce antiganglioside antibodies in mice and humans, providing information as to the possible risk of developing AMAN following these vaccinations. Inactivated A/H1N1pdm split vaccines (without adjuvant) used during the Japan 2009–2010 …