The Quality of Spousal Social Support as a Moderator of the Associations Between Child Maltreatment Severity and Adult Trauma Symptoms

Child maltreatment has been linked to a myriad of long-term difficulties, including trauma symptomatology. However, not all victims experience long-term distress. Thus, a burgeoning area of research focuses on factors that may impede or facilitate resiliency to the psychological correlates of child maltreatment. Specifically, the severity of the abusive acts may be associated with greater long-term difficulties. To date, however, with the exception of child sexual abuse, few studies have examined the severity of maltreatment as a risk factor in the development of trauma symptoms. In contrast, social support has been theorized to contribute to resiliency following abuse. However, to date, the majority of studies examining positive social support as a protective factor have relied on self-report measures of perceived social support, rather than observational measures of received social support. Moreover, no study to date has examined the role that negative social support (i.e, blaming, criticizing) may play in potentiating trauma symptoms among victims of child maltreatment. Because child maltreatment involves serious boundary violations by a trusted person, a marital relationship is an important domain in which to examine these constructs. That is, it may serve as an arena for the manifestation of psychological disturbances related to maltreatment. Thus, the present study examined whether observationally measured positive and negative spousal social support moderated the relationship between child maltreatment severity (i.e., sexual, physical, psychological abuse; neglect) and trauma symptomatology in women and men. Results indicated that the severity of each type of child maltreatment significantly predicted increased adult trauma symptomatology. Contrary to hypothesized outcomes, positive spousal social support did not predict decreased trauma symptomatology. However, negative spousal social support generally did predict increased trauma symptomatology. There were no consistent patterns of interactions between child maltreatment severity and either type of social support. Future directions for research will be discussed and clinical implications with regard to the intrapersonal and interpersonal functioning of child maltreatment victims will be highlighted.

INFLUENCE OF TYPE 2 BOVINE VIRAL DIARRHEA VIRUS NPRO ON ENHANCEMENT OF BOVINE RESPIRATORY SYNCYTIAL VIRUS REPLICATION MEDIATED BY ANTAGONISM OF HOST CELL INTERFERON TYPE I RESPONSES

Bovine viral diarrhea virus (BVDV) is a member of the genus Pestivirus, Family Flaviviridae. The virus can infect many species of animals of the order Artiodactyla. The BVDV genome encodes an auto protease, Npro, that degrades interferon regulatory factor-3 (IRF-3) reducing type I interferon (IFN-I) production from host cells. Bovine respiratory syncytial virus (BRSV) is a member of the genus Pneumovirus, Family Paramyxoviridae. Concurrent infection with BVDV and BRSV causes more severe respiratory and enteric disease than infection with either virus alone. Our hypothesis was that Npro modulates the innate immune responses to BVDV infection and enhances replication of BVDV or BRSV co-infection. The noncytopathic BVDV2 viruses NY93/c N- Npro 18 EGFP (a mutant with modified Npro fused with enhanced green fluorescent protein), NY93 infectious clone (NY93/c), wild-type NY93-BVDV2 (NY93-wt), and BRSV were evaluated in this study. The objectives of this study were: (1) to characterize the replication kinetics and IFN-I induction in Madin-Darby bovine kidney (MDBK) cells following infection with each of the BVDV isolates, and (2) to characterize the influence of BVDV-mediated IFN-I antagonism on enhancement of BRSV replication in bovine turbinate (BT) cells. NY93/c N- Npro 18 EGFP replicated 0.4 – 1.6 TCID50 logs lower than NY93-wt in MDBK cells. NY93/c N- Npro 18 EGFP-infected MDBK cells synthesized IFN-I significantly higher than NY93/c- and NY93-wt-infected MDBK cells. BT cells co-infected with NY93/c N- Npro 18 EGFP/BRSV or NY93-wt/BRSV were evaluated to determine the effects of co-infection on BRSV replication and IFN-I induction in BT cells. BRSV RNA levels in NY93-wt/BRSV co-infected BT cells were 2.49, 2.79, and 2.89 copy number logs significantly greater than in NY93/c N- Npro 18 EGFP/BRSV co-infected BT cells on days 5, 7, and 9 post-infection, respectively. BVDV RNA levels in NY93/c N- Npro 18 EGFP-infected BT cells were 1.64 – 4.38 copy number logs lower than in NY93-wt-infected BT cells. NY93/c N- Npro 18 EGFP single and co-infected BT cells synthesized IFN-I significantly higher than NY93-wt single and co-infected BT cells. In summary, these findings suggest: (1) NY93/c N- Npro 18 EGFP BVDV2 induced higher levels of IFN-I than BVDV2-wt and may be useful as a safer, replicating BVDV vaccine, and (2) Enhancement of BRSV infection by BVDV co-infection is mediated by antagonism of IFN-I.