No reports in the literature exist on the validity of self-swab for longitudinal studies of influenza virus infection and illness in Figure 1 . A-D, Molecular viral loads on first and third measurements (circles ) and second measurement (crosses ) for influenza A from the Influenza Resistance Information Study (IRIS) (A ) and the household transmission study (HTS) (B ) and for influenza B from the IRIS (C ) and the HTS (D ). E-H, Difference between observed and expected molecular viral load (VL) at the second measurement, with a histogram summarizing the differences, for influenza A from the IRIS (E ) and the HTS (F ) and for influenza B from the IRIS (G ) and the HTS (H ). The second measurement (crosses ) was collected by self-swab in the IRIS (A, C, E, G ) and by a healthcare professional in the HTS (B, D, F, H ). For the IRIS, the lower limit of detection (LLOD) of the influenza A assay was 54 viral particles per milliliter (vp/mL), and the lower limit of quantification (LLOQ) was 131 vp/mL; the LLOD of the influenza B assay was 168 vp/mL, and the LLOQ was 194 vp/mL. For the HTS, the LLOD of the influenza A and B assays was 550 copies/mL, and the LLOQ was 900 copies/mL. a community setting. Because of the need for multiple sequential respiratory specimens over the course of illness, such studies typically require multiple clinic visits by the patients or multiple home visits by the HCPs and are thus costly and complicated, which may also affect study compliance. Self-swab would thus be an attractive alternative, and further validation of this approach would benefit the design of future community-based studies. Further studies employing collection of NTSs by both the patients and HCPs in a parallel or randomized fashion could help to enable finer calibration of the measurements obtained by self-swabs. Molecular Mimicry as a Mechanism of Autoimmune Disease A variety of mechanisms have been suggested as the means by which infections can initiate and/or exacerbate autoimmune diseases. One mechanism is molecular mimicry, where a foreign antigen shares sequence or structural similarities with self-antigens. Molecular mimicry has typically been characterized on an antibody or T cell level. However, structural relatedness between pathogen and self does not account for T cell activation in a number of autoimmune diseases. A proposed mechanism that could have been misinterpreted for molecular mimicry is the expression of dual T cell receptors (TCR) on a single T cell. These T cells have dual reactivity to both foreign and self-antigens leaving the host vulnerable to foreign insults capable of triggering an autoimmune response. In this review, we briefly discuss what is known about molecular mimicry followed by a discussion of the current understanding of dual TCRs. Finally, we discuss three mechanisms, including molecular mimicry, dual TCRs, and chimeric TCRs, by which dual reactivity of the T cell may play a role in autoimmune diseases. Chronic autoimmune diseases are the by-product of the immune system recognizing self-antigens as foreign, which can lead to inflammation and destruction of specific tissues and organs (immunopathology) [1] . The impact of these diseases is global and heterogeneous with over 100 million people afflicted with more than 80 different autoimmune diseases [2] . While the etiology of autoimmune diseases is not fully elucidated, the causes are likely based on a combination of hereditary and environmental factors [3] . Although host genetic background contributes to the induction of an immune response to self, epidemiological and molecular evidence implicates infectious agents (viral and bacterial) as the principal environmental insults responsible for the induction of autoimmune diseases (reviewed in [4] [5] [6] ). Prolonged proinflammatory responses to infections have been associated with the initiation and exacerbation of autoimmune diseases (reviewed in [4, 7, 8] ). Inflammation is facilitated by proinflammatory cytokines such as type I interferon (IFN), interleukin (IL)-1β, IL-12, IFN-γ, IL-17, and tumor necrosis factor (TNF)-α (reviewed in [7, 9, 10] ). However, these proinflammatory cytokines are critical for clearance of pathogens, suggesting that environmental factors are able to divert the immune response towards immunopathogenesis. Although a number of immune cells are responsible for secreting proinflammatory cytokines, the primary cell types implicated in a vast majority of autoimmune disorders are autoreactive B and T cells, or antibody recognition of self [11] . Although a number of viruses and bacteria have been linked to the initiation of certain autoimmune diseases, identifying a particular virus or bacteria that is solely responsible for the induction of an autoimmune response is rare. This occurrence is due to the potential for multiple infections being involved in priming the immune system and other infections triggering disease, which could explain why no one viral infection has been conclusively linked to the development of immune-mediated autoimmune diseases [7] . However, there are a variety of examples of bacterial infections initiating and exacerbating autoimmune diseases. Streptococcus pyogenes is a gram-positive bacterium which causes group A streptococcal infection that is responsible for a number of diseases. The complications associated with S. pyogenes are rheumatic fever and glomerulonephritis. The infection causes the production of cross-reactive antibodies in response to the bacteria. Antibodies recognize the M protein (virulence factor) and the N-acetyl-β-Dglucosamine (GLcNAc) of S. pyogenes and cross-react with myosin leading to heart damage (reviewed in [8, 12, 13] ). Further evidence of molecular mimicry due to the production of cross-reactive antibody includes infection with gram-negative bacteria, such as Klebsiella pneumoniae and Campylobacter jejuni. Infection with K. pneumonia or C. jejuni leads to the production of cross-reactive antibodies able to recognize the self-antigens histocompatibility leukocyte antigen (HLA)-B27 and gangliosides, which induce ankylosing spondylitis and Guillain-Barré syndrome, respectively (reviewed in [8, 14] ). Examples of human autoimmune diseases with possible links with molecular mimicry are presented in Table 1 .