Background Rate of corrective nasal surgery after maxillomandibular advancement (MMA) for obstructive sleep apnea (OSA) has been reported to be 18.7% for functional and aesthetic indications. Objective Describe a comprehensive strategy to optimize nasal outcomes with MMA for OSA. Methods A retrospective review of patients undergoing MMA for OSA in a tertiary referral center was performed, with a comprehensive perioperative intervention to optimize nasal outcomes from January 2014 to February 2018. Outcomes included the Apnea-Hypopnea Index (AHI), oxygen saturation (SpO2) nadir, corrective nasal surgery needed after MMA, and Nasal Obstruction Symptom Evaluation (NOSE) scores. Results AHI after MMA showed significant reduction (-34.65, p  less then  0.001), SpO2 nadir increased (+6.08, p  less then  0.001), and NOSE scores decreased (-5.96, p  less then  0.001). Corrective nasal surgery needed after MMA was reported in 6.5% (8 of 122) subjects at a mean of 8.5 months, ranging from 1 to 24.7 months. Six subjects underwent either septoplasty and/or valve stenosis repair, and two subjects underwent functional and aesthetic rhinoplasty. Conclusion A perioperative strategy was applied since 2014 that showed effectiveness in reducing post-MMA corrective nasal surgery to 6.5%.Understanding the earliest events of HIV sexual transmission is critical to develop and optimize HIV prevention strategies. To gain insights into the earliest steps of HIV rectal transmission, including cellular targets, rhesus macaques were intra-rectally challenged with a single-round SIV-based dual reporter that expresses luciferase and iRFP670 upon productive transduction. The vector was pseudotyped with the HIV-1 envelope JRFL. Regions of tissue containing foci of luminescent, transduced cells were identified macroscopically using an in vivo imaging system, and individual transduced cells expressing fluorescent protein were identified and phenotyped microscopically. This system revealed that anal and rectal tissues are both susceptible to transduction 48 hours after the rectal challenge. Detailed phenotypic analysis revealed that on average, 62% of transduced cells are CCR6+ T cells-the vast majority of which express RORγT, a Th17 lineage-specific transcription factor. The second most common target cells were immature dendritic cells at 20%. These two cell types were transduced at the rates that are four to five times higher than their relative abundances indicate. Our work demonstrates that Th17 T and immature dendritic cells are preferential initial targets of HIV/SIV rectal transmission. IMPORTANCE Men and women who participate in unprotected receptive anal intercourse are at high risk for acquiring HIV. While in vitro data have developed a framework for understanding HIV cell tropism, the initial target cells in the rectal mucosa have not been identified. In this study, we identify these early host cells by using an innovative rhesus macaque rectal challenge model and methodology, which we previously developed. Thus, by shedding light on these early HIV/SIV transmission events, this study provides a specific cellular target for future prevention strategies.Uncoordinated 51-like kinase 1 (ULK1) is a well-characterized initiator of canonical autophagy under basal or pathological conditions. Porcine haemagglutinating encephalomyelitis virus (PHEV), a neurotropic betacoronavirus (β-CoV), impairs ULK1 kinase but hijacks autophagy to facilitate viral proliferation. However, the machinery of PHEV-induced autophagy initiation upon ULK1 kinase deficiency remains unclear. Here, the time course of PHEV infection showed a significant accumulation of autophagosomes (APs) in nerve cells in vivo and in vitro. Utilizing the ULK1-knockout neuroblastoma cells, we have identified that ULK1 was not essential for productive AP formation induced by PHEV. In vitro phosphorylation studies discovered that mTORC1-regulated ULK1 activation stalls during PHEV infection, whereas the AP biogenesis was controlled by AMPK-driven BECN1 phosphorylation. BAY 1217389 A lack of BECN1 is sufficient to block LC3 lipidation and disrupt recruitment of the LC3-ATG14 complex. Moreover, BECN1 acts as a bona fide subV infection, where productive autophagosome (AP) biogenesis bypassing the multifaceted regulation of ULK1 kinase. The PHEV-triggered non-canonical autophagy underscores the complex interactions of virus-host, and will help in the development of therapeutic strategies targeting non-canonical autophagy to treat β-CoV disease.DDX17 is a member of the DEAD-Box helicase family proteins involved in cellular RNA folding, splicing, and translation. It has been reported that DDX17 serves as a co-factor of host zinc finger antiviral protein (ZAP)-mediated retroviral RNA degradation and exerts direct antiviral function against Raft Valley Fever Virus though binding to specific stem-loop structures of viral RNA. Intriguingly, we have previously shown that ZAP inhibits Hepatitis B virus (HBV) replication through promoting viral RNA decay, and the ZAP-responsive element (ZRE) of HBV pregenomic RNA (pgRNA) contains a stem-loop structure, specifically epsilon, which serves as the packaging signal for pgRNA encapsidation. In this study, we demonstrated that the endogenous DDX17 is constitutively expressed in human hepatocyte-derived cells but dispensable for ZAP-mediated HBV RNA degradation. However, DDX17 was found to inhibit HBV replication primarily by reducing the level of cytoplasmic encapsidated pgRNA in a helicase-dependent manner. Immuniviral factor through interacting with viral RNA. In this study, we, for the first time, demonstrate that DDX17 inhibits HBV through blocking the formation of viral replication complex, which not only broadens the antiviral spectrum of DDX17, but also provides new insight into the molecular mechanism of DDX17-mediated virus-host interaction.Latent HIV reservoirs persist in people living with HIV despite effective antiretroviral therapy and contribute to rebound viremia upon treatment interruption. Macrophages are an important reservoir cell-type, but analysis of agents that modulate latency in macrophages is limited by lack of appropriate in vitro models. We therefore generated an experimental system to investigate this by purifying non-productively-infected human monocyte-derived macrophages (MDM) following in vitro infection with an M-tropic EGFP reporter HIV clone, and quantified activation of HIV transcription using live-cell fluorescence microscopy. The proportion of HIV-infected MDM was quantified by qPCR detection of HIV DNA, and GFP expression was validated as a marker of productive HIV infection by co-labelling of HIV Gag protein. HIV transcription spontaneously reactivated in latently-infected MDM at a rate of 0.22% ± 0.04 cells per day (mean ± SEM, n=10 independent donors), producing infectious virions able to infect heterologous T cells in coculture experiments, and both T cells and TZM-bl cells in a cell-free infection system using MDM culture supernatants.