Virus and Allergy: Immunoglobulin E (IgE) and IgG2a Response to Sendai Virus (SeV) Infection in C57BL6/J Mice

Increased tendency to develop infantile or childhood asthma is not well understood. Several factors during infancy appear to impact the development of asthma later in childhood. These variations include cytokine profiles, heritability, pre and post-natal environment, including exposure to allergens and microbes, and viral Infections. Traditionally allergic stimuli have been thought to lead to the development of asthma. However, it is now clear that some viral infections may lead to the development of asthma. Human Respiratory Syncytial Virus (RSV), of the family paramyxoviridae, subfamily pneumovirinae, causes a statistically significant increase in asthma in children experiencing severe infections. The paramyxoviridae viral family infects several mammalian species. Mouse Parainfluenza Virus Type 1, or Sendai Virus (SeV), models human RSV infection in mice. Common immune responses to intracellular pathogens like viruses are characterized a T_H1 immune response. This pathway leads to production of IgG2a and normally is not associated with asthma-like symptoms. The allergic response (a T_H2 pathway) is characterized by production of Immunoglobulin E (IgE) and asthma-like symptoms. Thus, long-term elevated levels of IgE post-infection may indicate an allergic response or even development of allergy as a result of the viral insult. Since SeV causes an asthma-like (hyperreactive airway and goblet cell hyperplasia) response in mice, it was hypothesized that the infection might also increase IgE levels. Therefore, the response of these two antibodies to SeV infection was evaluated to determine if there was both an allergic-type and anti-viral antibody response. This experiment utilized Enzyme-linked Immunosorbent Assays (ELISAs) to quantify IgE and IgG2a levels in infected and control C57BL6/J mice. The results show a marked increase in both total IgE and total IgG2a levels, perhaps indicating both a T_H1 and T_H2 response. The time scale of the IgE response is of particular interest: virus is not detectable by PCR between 12 and 21 days after infection, but a significant increase in IgE levels does not occur until day 21. Further experiments are required to determine whether this is a specific or nonspecific IgE response to SeV. However, the increase in IgE indicates that SeV (an intracellular pathogen) stimulates a T_H2 response, and supplies evidence linking viral infection to allergic disease.