Systemic cytomegalovirus masquerading as a colorectal mass in a patient with undiagnosed HIV/AIDS.

Introduction: Cytomegalovirus (CMV) infection is common among patients with human immunodeficiency virus (HIV) infection. Gastrointestinal (GI) involvement with tumor like lesion is a rare presentation. Our patient presented with rectal pain and findings concerning for malignancy. Subsequently our patient was diagnosed with acquired immunodeficiency syndrome (AIDS), CMV viremia and CMV proctitis. Case: A 37-year-old man who reported having sex with men presented with severe proctalgia and hematochezia. Imaging showed irregular rectal wall thickening concerning for malignancy. Sigmoidoscopy revealed a circumferential necrotic lesion suspicious for malignancy. Surprisingly, biopsy showed a cytopathic effect compatible with CMV infection. In addition to testing positive for CMV, patient was newly diagnosed with HIV/AIDS, hepatitis C, syphilis, and gonorrhea. CMV infection was treated with ganciclovir, which resulted in a significant response. Ganciclovir was later replaced with valganciclovir. Valganciclovir was continued and antiretroviral therapy (ART) was started as an outpatient and with resolution of symptoms. Discussion: CMV infection is one of the most common opportunistic infections among patients with HIV infection. Several cases of CMV colitis were reported among immunocompromised patients. Our patient's presenting symptoms and direct visualization of rectal lesion were not only deceptive but also unique. As what looked like a rectal malignancy was later diagnosed as tissue invasive CMV by biopsy. Invasive CMV infection should be managed with ganciclovir. Conclusion: GI CMV as the initial presentation of HIV is rare. Moreover, CMV proctitis can masquerade as a rectal cancer and clinicians should be aware of this rare presentation of CMV.

Oligodendrocyte precursor cells present antigen and are cytotoxic targets in inflammatory demyelination.

Oligodendrocyte precursor cells (OPCs) are abundant in the adult central nervous system, and have the capacity to regenerate oligodendrocytes and myelin. However, in inflammatory diseases such as multiple sclerosis (MS) remyelination is often incomplete. To investigate how neuroinflammation influences OPCs, we perform in vivo fate-tracing in an inflammatory demyelinating mouse model. Here we report that OPC differentiation is inhibited by both effector T cells and IFNγ overexpression by astrocytes. IFNγ also reduces the absolute number of OPCs and alters remaining OPCs by inducing the immunoproteasome and MHC class I. In vitro, OPCs exposed to IFNγ cross-present antigen to cytotoxic CD8 T cells, resulting in OPC death. In human demyelinated MS brain lesions, but not normal appearing white matter, oligodendroglia exhibit enhanced expression of the immunoproteasome subunit PSMB8. Therefore, OPCs may be co-opted by the immune system in MS to perpetuate the autoimmune response, suggesting that inhibiting immune activation of OPCs may facilitate remyelination.