The post-2009 influenza pandemic era : time to revisit antibody immunodominance

The current inactivated influenza vaccines rely on the induction of neutralizing antibodies against the head domain of the viral hemagglutinin (HA). The HA head contains five immunodominant antigenic sites, all of which are subject to antigenic drift, thereby limiting vaccine efficacy. Bypassing the immune system's tendency to focus on the most variable regions of the HA may be a step toward more broadly protective influenza vaccines. However, this requires a better understanding of the biological meaning of immunodominance, and of the hierarchy between different antigenic sites. In this issue of the JCI, Liu et al. determined the immunodominance of the five antigenic sites of the HA head in experimentally infected mice, guinea pigs, and ferrets. All three species exhibited different preferences for the five sites of the 2009 pandemic H1N1 strain. Moreover, human subjects exhibited yet a different pattern of immunodominance following immunization with the standard inactivated influenza vaccine. Together, these results have important implications for influenza vaccine design and interpretation of animal models

Apoptosis in the lungs of pigs infected with porcine reproductive and respiratory syndrome virus and associations with the production of apoptogenic cytokines

International audienceApoptosis was studied in the lungs of pigs during an infection with a European strain of porcine reproductive and respiratory syndrome virus (PRRSV) and it was examined if cytokines were involved in the induction of apoptosis. Twenty-two 4- to 5-week-old gnotobiotic pigs were inoculated intranasally with 10$^{6.0}$ TCID$_{50}$ of the Lelystad virus and euthanised between 1 and 52 days post inoculation (PI). The lungs and broncho-alveolar lavage (BAL) cells were assessed both for virus replication and apoptosis; BAL fluids were examined for interleukin (IL)-1, tumour necrosis factor-alpha and IL-10. Double-labellings were conducted to determine the relation between virus replication and apoptosis and to identify the apoptotic cells. Apoptosis occurred in both infected and non-infected cells. The percentages of infected cells, which were apoptotic, ranged between 9 and 39% in the lungs and between 13 and 30% in the BAL cells. The majority of apoptotic cells were non-infected. Non-infected apoptotic cells in the lungs were predominantly monocytes/macrophages, whereas those in the broncho-alveolar spaces were predominantly lymphocytes. The peak of apoptosis in the lungs at 14 days PI was preceded by a peak of IL-1 and IL-10 production at 9 days PI, suggesting a possible role of these cytokines in the induction of apoptosis in non-infected interstitial monocytes/macrophages. However, the latter hypothesis was not confirmed in vitro, since blood monocytes or alveolar macrophages did not undergo apoptosis after treatment with recombinant porcine IL-1 or IL-10

Serosurvey for viruses associated with reproductive failure in newly introduced gilts and in multiparous sows in Belgian sow herds

A serosurvey for viruses associated with reproductive disorders was conducted in 25 conventional Belgian farms. Serum antibody titers for porcine reproductive and respiratory syndrome virus (PRRSV), porcine circovirus type 2 (PCV2), porcine parvovirus (PPV), porcine enteroviruses (PEV) and swine influenza viruses (SIV) were determined in gilts and sows. All the animals were seropositive for PCV2 and >95% were seropositive for all 4 embryopathogenic PEV serotypes. Consequently, special preventive measures appear to be unnecessary for these viruses. In I farm, non-vaccinated gilts were found to run a risk of developing PPV-induced reproductive disorders. Vaccination against PPV could exclude this risk. In 10 farms, gilts seronegative for one or more specific SIV subtypes were introduced into a herd that had previously been infected with the same subtypes. Vaccination of gilts against SIV may prevent reproductive disorders in gilts and respiratory problems in their offspring. In I farm, newly purchased gilts that were possibly shedding PRRSV were introduced into a PRRSV seronegative sow herd. Serological screening prior to purchase or vaccination of the sows could have resolved this dangerous situation