Pharmaceuticals and, as such, receive salary and benefits, including ownership of stock and stock options. KM receives grants and consulting fees from Inovio Pharmaceuticals related to DNA vaccine development. DBW has received grant funding, participates in industry collaborations, has received speaking honoraria, and has received fees for consulting, including serving on scientific review committees and board series. Remuneration received by DBW includes direct payments, stock, or stock options, and, in the interest of disclosure, he notes potential conflicts associated with his work with Inovio Pharmaceuticals and possibly others. MCW and DBW have a pending US patent, 62750213.

Venezuelan equine encephalomyelitis (VEE) viruses, of the genus Alphavirus of the family Togaviridae, cause disease ranging from mild febrile reactions to fatal encephalitic zoonoses in Equidae and humans. They are transmitted by haematophagous insects, primarily mammalophilic mosquitoes. The VEE complex of viruses includes six antigenic subtypes (I-VI). Within subtype I there are five antigenic variants (variants AB-F). Originally, subtypes I-A and I-B were considered to be distinct variants, but they are now considered to be identical (I-AB). Antigenic variants I-AB and I-C are associated with epizootic activity in equids and human epidemics. Historically, severe outbreaks have involved many thousands of human and equine cases. The other three variants of subtype I (I-D, I-E, IF) and the other five subtypes of VEE (II-VI) circulate in natural enzootic cycles. Equidae serve as amplifying hosts for epizootic VEE strains while enzootic VEE viruses cycle primarily between sylvatic rodents and mosquitoes. Enzootic variants and subtypes have been considered to be nonpathogenic for equids, but can cause clinical disease in humans. During 1993 and 1996 however, limited outbreaks of encephalitis in horses in Mexico were shown to be caused by enzootic VEE viruses of subtype I-E. Identification of the agent: Diagnosis of VEE virus infection can be confirmed by the isolation, identification, and antigenic classification of the isolated virus.

Several different assay methodologies have been described for the evaluation of HIV or SIV‐specific antibody‐dependent cell‐mediated cytotoxicity (ADCC). Commonly used assays measure ADCC by evaluating effector cell functions, or by detecting elimination of target cells. Signaling through Fc receptors, cellular activation, cytotoxic granule exocytosis, or accumulation of cytolytic and immune signaling factors have been used to evaluate ADCC at the level of the effector cells. Alternatively, assays that measure killing or loss of target cells provide a direct assessment of the specific killing activity of antibodies capable of ADCC. Thus, each of these two distinct types of assays provides information on only one of the critical components of an ADCC event; either the effector cells involved, or the resulting effect on the target cell. We have developed a simple modification of our previously described high‐throughput ADCC GranToxiLux (GTL) assay that uses area scaling analysis (ASA) to facilitate simultaneous quantification of ADCC activity at the target cell level, and assessment of the contribution of natural killer cells and monocytes to the total observed ADCC activity when whole human peripheral blood mononuclear cells are used as a source of effector cells. The modified analysis method requires no additional reagents and can, therefore, be easily included in prospective studies. Moreover, ASA can also often be applied to pre‐existing ADCC‐GTL datasets. Thus, incorporation of ASA to the ADCC‐GTL assay provides an ancillary assessment of the ability of natural and vaccine‐induced antibodies to recruit natural killer cells as well as monocytes against HIV or SIV; or to any other field of research for which this assay is applied. © 2018 The Authors. Cytometry Part A published by Wiley Periodicals, Inc. on behalf of ISAC.

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Maternal vaccination to induce anti-HIV immune factors in breast milk is a potential intervention to prevent postnatal HIV-1 mother-to-child transmission (MTCT). We previously demonstrated that immunization of lactating rhesus monkeys with a modified vaccinia More than 200,000 new pediatric human immunodeficiency virus (HIV) infections occur annually via mother-to-child transmission (MTCT), nearly half through breastfeeding (1). Antiretroviral (ARV) drugs can dramatically reduce the rate of MTCT, but in areas of high HIV prevalence, acute HIV infection in pregnant and postpartum women as well as poor access and adherence to ARV treatment throughout the breastfeeding period has limited progress in the prevention of breast milk transmission (2). According to UNAIDS in 2014, only 68% of HIV-infected pregnant women in low-and middle-income countries received ARV therapy during pregnancy, and only 61% of those women continued this therapy postpartum (3). Despite the risk of HIV acquisition, breastfeeding is necessary for infant survival in many regions of the world, as breastfed infants have lower rates of diarrheal and respiratory infections (4). It is well established that antibodies are transferred to infants via the placenta and through breast milk consumption (5); thus, maternal immunization could