Despite a high coverage rate with two doses of mumps-containing vaccine, a large mumps outbreak occurred, characterized by two-dose vaccine failure, particularly among midwestern college-age adults who probably received the second dose as schoolchildren. A more effective mumps vaccine or changes in vaccine policy may be needed to avert future outbreaks and achieve the elimination of mumps.

The epidemiologic features of this outbreak suggest that intense exposures, particularly among boys in schools, facilitated transmission and overcame vaccine-induced protection in these patients. High rates of two-dose coverage reduced the severity of the disease and the transmission to persons in settings of less intense exposure.

Despite high community vaccination coverage, measles outbreaks can occur among clusters of intentionally undervaccinated children, at major cost to public health agencies, medical systems, and families. Rising rates of intentional undervaccination can undermine measles elimination.

Vaccination with formalin-inactivated respiratory syncytial virus (FI-RSV) vaccine or RSV G glycoprotein results in enhanced pulmonary disease after live RSV infection. Enhanced pulmonary disease is characterized by pulmonary eosinophilia and is associated with a substantial inflammatory response. We show that the absence of the G glycoprotein or G glycoprotein CX3C motif during FI-RSV vaccination or RSV challenge of FI-RSV-vaccinated mice, or treatment with anti-substance P or anti-CX3CR1 antibodies, reduces or eliminates enhanced pulmonary disease, modifies T-cell receptor V␤ usage, and alters CC and CXC chemokine expression. These data suggest that the G glycoprotein, and in particular the G glycoprotein CX3C motif, is key in the enhanced inflammatory response to FI-RSV vaccination, possibly through the induction of substance P.Respiratory syncytial virus (RSV) is the most common cause of lower respiratory tract infections in infants and young children (1,50,54,59). RSV can also cause serious lower respiratory tract disease in patients of any age with compromised immune, respiratory, or cardiac systems (7,13,14,20,26,60,62). Despite the importance of RSV as a respiratory pathogen, there is presently no safe and effective RSV vaccine available. The first RSV vaccine trial with a formalin-inactivated RSV (FI-RSV) vaccine yielded disastrous results in young vaccinees who were subsequently naturally infected with RSV, as many developed enhanced pulmonary disease leading to hospitalization, and even to death in a few vaccine recipients (5,17,73). This outcome prompted investigators to search for viral and/or host factors that may contribute to enhanced disease in the effort to ensure that RSV vaccines would be safe.Studies with BALB/c mice have provided some indication of the mechanisms that may have contributed to FI-RSV-enhanced pulmonary disease. BALB/c mice vaccinated with vectors expressing G glycoprotein, purified G glycoprotein, or FI-RSV develop extensive enhanced pulmonary disease characterized by pulmonary eosinophilia, weight loss, exaggerated Th2-type cytokine responses, selective priming of V␤14 ϩ CD4ϩ T cells, and augmented substance P (SP) expression when challenged with RSV (23,27,51,68,70,71). Interestingly, the soluble form of the G glycoprotein has been shown to be most effective at sensitizing for enhanced disease (34, 35). Studies from our laboratory comparing the immune responses to infection with wild-type RSV or an RSV mutant lacking the G and SH genes have shown that RSV G and/or SH glycoprotein expression alters pulmonary trafficking of innate immune cells (CD11b ϩ cells, polymorphonuclear cells [PMN], and NK cells), Th1-and Th2-type cytokine patterns, and CC and CXC chemokine mRNA expression by bronchoalveolar lavage (BAL) cells and is associated with increased pulmonary SP expression (64,67,68). In addition, recent studies from our laboratory have shown that the G glycoprotein contains a CX3C chemokine motif that interacts with the CX3C chemokine receptor CX3CR1, induces leukocyte chemo...

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The external expert panel concluded that the elimination of endemic measles, rubella, and CRS from the United States was sustained through 2011. However, international importation continues, and health care providers should suspect measles or rubella in patients with febrile rash illness, especially when associated with international travel or international visitors, and should report suspected cases to the local health department.

Respiratory syncytial virus (RSV) infection in the neonate can alter respiratory rates, i.e., lead to episodes of apnea. We show that RSV G glycoprotein reduces respiratory rates associated with the induction of substance P (SP) and G glycoprotein-CX3CR1 interaction, an effect that is inhibited by treatment with anti-G glycoprotein, anti-SP, or anti-CX3CR1 monoclonal antibodies. These data suggest new approaches for treating some aspects of RSV disease.Respiratory syncytial virus (RSV) is recognized as the most important cause of serious lower respiratory tract illness in infants and young children worldwide (17). Most children are infected with RSV by age two, and repeated infections can occur throughout life, with serious complications most often occurring in elderly patients and patients with compromised cardiac, immune, or pulmonary systems (7,8,10,13,38). RSV infection in infants and young children is often associated with bronchiolitis and an increase in respiratory rates; apnea can also occur (3). In one study of 274 infants under 6 months of age, 56 infants (20.4%) had apnea with RSV infection (3). The mechanisms by which RSV infection causes apnea are not understood. One potential mechanism for RSV-associated alteration in respiratory rates is induction of pulmonary substance P (SP). SP has been associated previously with excitatory effects related to respiratory rates (1, 2, 9, 12, 28), and pulmonary levels of SP are increased during RSV infection in the BALB/c mouse (46). In addition, there is some indication that SP has an important role in bronchial hypersensitivity reactions in children (25), and elevated levels of tachykinins have been recovered from the airways of patients with asthma and chronic obstructive pulmonary disease (18,31,42). RSV is the predominant cause of bronchiolitis (29), and bronchiolitis has clinical features of obstructed airway disease. SP is present in sensory, parasympathetic, and sympathetic neurons in airways and has been shown elsewhere to have proinflammatory effects on immune cells and to mediate mucus production, vascular leakage or edema, and smooth muscle contraction (5,23,30,32,33,36). In the mouse model, induction of SP during RSV infection appears to be related to the presence of RSV G and/or SH glycoprotein (46). The RSV G glycoprotein has been shown elsewhere to be associated with a number of proinflammatory effects (43,45,46) and may contribute to the pathogenesis of RSV disease in several ways. Studies of mice have shown that RSV G glycoprotein modifies chemokine (43) and cytokine (45) expression, alters pulmonary leukocyte recruitment (45), and sensitizes for pulmonary eosinophilia (11,40,41). BALB/c mice immunized with vaccinia virus expressing G glycoprotein, purified G glycoprotein, or formalin-treated RSV produce an exaggerated CD4 ϩ T-cell response with increased Th2-type cytokine expression and pulmonary eosinophilia when challenged with RSV (11,27).Structurally, the RSV G glycoprotein is of particular interest as it contains a CX3C motif at amino acid...

Case patients generally had lower preoutbreak mumps antibody levels than nonpatients. However, titers overlapped and no cutoff points separated all mumps case patients from all nonpatients.