Influenza vaccine provides protection against infection with matched strains, and this protection correlates with serum antibody titres. In addition to antibodies, influenza-specific CD8+ T-lymphocyte responses are important in decreasing disease severity and facilitating viral clearance. Because this response is directed at internal, relatively conserved antigens, it affords some cross-protection within a given subtype of influenza virus. With the possibility of a broader A(H1N1) Mexico outbreak in the fall of 2009, it appeared worthwhile studying the degree of cellular immune response-mediated cross-reactivity among influenza virus isolates. The composition of the 2006-2007 influenza vaccine included the A/New Caledonia/20/1999 strain (comprising a virus that has been circulating, and was included in vaccine preparations, for 6-7 years) and two strains not previously included (Wisconsin and Malaysia). This combination afforded us the opportunity to determine the degree of cross-reactive cellular immunity after exposure to new viral strains. We analysed the antibody responses and the phenotype and function of the T cell response to vaccine components. The results obtained show that antibody responses to A/New-Caledonia were already high and vaccination did not increase antibody or cytotoxic T lymphocyte responses. These data suggest that repeated exposure to the same influenza stain results in limited boosting of humoral and cellular immune responses.

Avian pneumovirus subgroup C (APV/C) has recently been reported to be more closely related to human metapneumovirus (hMPV) as determined by sequence analysis. To examine the antigenic relationship between APV/C and hMPV, the APV/C fusion (F) gene was cloned and expressed as an uncleaved glycoprotein in a baculovirus system. The reactivity of the APV/C F protein with antibodies against APV subgroups A, B, C, and hMPV was examined by Western blot analysis. The results showed that the expressed APV/C F protein was not only recognized by APV/C-specific antibodies but also by antibodies raised against hMPV. Previously expressed recombinant hMPV F protein also reacted with APV/C-specific antibodies, suggesting that there was significant antigenic cross-reactivity and a potential evolutionary relationship between hMPV and APV/C. Interestingly, the recombinant F proteins from APV/C and hMPV were not recognized by polyclonal antibodies specific to APV subgroups A and B.

Despite growing recognition of the importance of social, economic, and political contexts for population health and health inequalities, research on pain disparities relies heavily on individual-level data, while neglecting overarching macrolevel factors such as state-level policies and characteristics. Focusing on moderate or severe arthritis-attributable joint pain—a common form of pain that considerably harms individuals' quality of life—we (1) compared joint pain prevalence across US states; (2) estimated educational disparities in joint pain across states; and (3) assessed whether state sociopolitical contexts help explain these 2 forms of cross-state variation. We linked individual-level data on 407,938 adults (ages 25-80 years) from the 2017 Behavioral Risk Factor Surveillance System with state-level data on 6 measures (eg, the Supplemental Nutrition Assistance Program [SNAP], Earned Income Tax Credit, Gini index, and social cohesion index). We conducted multilevel logistic regressions to identify predictors of joint pain and inequalities therein. Prevalence of joint pain varies strikingly across US states: the age-adjusted prevalence ranges from 6.9% in Minnesota to 23.1% in West Virginia. Educational gradients in joint pain exist in all states but vary substantially in magnitude, primarily due to variation in pain prevalence among the least educated. At all education levels, residents of states with greater educational disparities in pain are at a substantially higher risk of pain than peers in states with lower educational disparities. More generous SNAP programs (odds ratio [OR] = 0.925; 95% confidence interval [CI]: 0.963-0.957) and higher social cohesion (OR = 0.819; 95% CI: 0.748-0.896) predict lower overall pain prevalence, and state-level Gini predicts higher pain disparities by education.

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