Herpes simplex virus 1 (HSV-1) infects the majority of the human population and can induce encephalitis, which is the most common cause of sporadic, fatal encephalitis. An increase of microglia is detected in the brains of encephalitis patients. The issues regarding whether and how microglia protect the host and neurons from HSV-1 infection remain elusive. Using a murine infection model, we showed that HSV-1 infection on corneas increased the number of microglia to outnumber those of infiltrating leukocytes (macrophages, neutrophils, and T cells) and enhanced microglia activation in brains. HSV-1 antigens were detected in brain neurons, which were surrounded by microglia. Microglia depletion increased HSV-1 lethality of mice with elevated brain levels of viral loads, infected neurons, neuron loss, CD4 T cells, CD8 T cells, neutrophils, interferon (IFN)-β, and IFN-γ. In vitro studies demonstrated that microglia from infected mice reduced virus infectivity. Moreover, microglia induced IFN-β and the signaling pathway of signal transducer and activator of transcription (STAT) 1 to inhibit viral replication and damage of neurons. Our study reveals how microglia protect the host and neurons from HSV-1 infection.
The IOP measured by the three methods--NCT, GAT, and PDCT--decreased as a result of the change in CCT induced by orthokeratology. The influence on NCT and GAT was greater than that on PDCT.
Carcinoma ex pleomorphic adenoma affects glandular structures, occurring mostly in major salivary glands and less commonly in the lacrimal gland. We present a rare case in the lacrimal gland. We highlight the importance of keeping this rare tumor in mind and the early detection of symptoms because such a malignant transformation could occur in pleomorphic adenomas, with the proportion dependent on the duration of the tumor.
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