 All right, I'm Lynn Hassmann, the UVITAS fellow. This is a case of multi-coccal corioratinitis and drenching fever. So this is a patient, a 63-year-old female with a five-day history of blurry vision in her right eye that followed a three-week history of a flu-like illness. So she has no significant past medical, ocular, or family history, but on review of systems, she has joint pain, muscle pain, fatigue, chills, night sweats. She has a follicular type of rash in her arms and legs. She has new frontal headaches, some neck stiffness, kind of some mental slowing, and sinus congestion. So she's obviously sick. Her exposure history is significant for some mosquito bites earlier this summer that the patient presented in the fall, and general HSV. So in the right eye, her vision is 2030. There's one-plus AC cell and a little bit of vitreous cell. And in the right fundus, you can see these round white lesions kind of along the arcades and then extending up above and down below. And it doesn't show well in this picture, but there's also some intra-retinal hemorrhages in the peripheral macula. The left eye, the vision is 2015. There's not really any AC or vitreous cell, but she has a few similar lesions kind of looking superiorly from the optic nerve into the superior periphery. Her fundus autofluorescence is normal in the center of the macula where she didn't have any spots. But along the inferior arcade, especially in the right eye, you can see there's kind of this hyper-autofluorescent lesion with a hypo-autofluorescent center. And if we zoom in a little bit, you can see there's that lesion. It kind of looks like a target. And then there's some other hyper- and hypo-autofluorescent changes in the area that we saw those white lesions. Her fluorescent angiography in the right eye, the more affected eye, shows an early blockage right there in the upper right frame. And then late staining, which is typical of an inflammatory lesion. And the left eye has pretty minimal changes. It probably did not showing up very well, but in the area where she had those white spots, there's also some staining. The ICG, we can also see these lesions on ICG. And following sort of a similar pattern in the right eye are on the superior and inferior arcades and branching out from there. And then in the left eye into the superior near periphery. So this imaging is basically showing us that the retina is involved. We see that on the fluorescein and that something is blocking this ICG signal either at the level of the RPE or deeper in the coroid. So the FAA and ICG lesions kind of corresponding. And you can see this pattern that's sort of following the arcades and then branching out. So on the OCT, the right eye, you can see starting at the top, the center of the macula, the fovea there looks pretty normal. The retinal architecture looks normal. There's not a lot of vitreous cell. You can see some early vitreous separation in the nasal side on your right and also some hyperreflectivity of the RNFL there. But then if we move down to the level of the inferior arcade where those lesions were in the right eye, you can see there's vitreous cell, there's vitreous separation, there's hyperreflectivity in the RNFL as well as along the RPE. You can see this kind of sort of clumps of hyperreflectivity at the level of the RPE and a loss of that overlying ellipsoid layer or the junction between the inner and outer segments of the photoreceptors. And then we have similar changes in the left eye of the less dramatic. The center fovea architecture is normal and then looking kind of superiorly in the left eye in this lower picture, you see some vitreous cell and RNFL hyperreflectivity. So the differential diagnosis for this patient based on that characteristic appearance of the lesions, sorry to everybody who took boards yesterday and this presentation's coming later, but this is West Nile virus, probably. But we always include some other infectious etiologies in our differential, particularly tuberculosis and syphilis. They can look a lot of different ways. Sarcoidosis would be an inflammatory process that could present in a multitude of ways and then inflammatory white dot syndromes, including mutes, PIC, multifocal corditis with panmubitis, acute posterior multifocal placoid pigment and apathy or ampy and azore. So her laboratory workup showed positive IgM and IgG for West Nile virus and negative workup otherwise. She had a mild thrombocytopenia probably going along with her acute febrile illness. So West Nile virus clinical infection, the incubation period for this disease is two to 14 days and it presents in patients in a variety of ways. The majority of people, 70 to 80% are totally asymptomatic. There's a mild febrile illness in about 20 to 30% and then there's neurologic disease in 1%. And neurologic disease is associated with a slightly older demographic, 40s to 60s, not really elderly by any means, but younger people are more likely to be asymptomatic. And then advanced stage and diabetes has also been associated with a more severe neurologic disease. So what do we see in the eye? 40 to 50% of patients with neurologic disease get a choreo-rhetonitis. And we see these classic targetoid lesions in multiple stages of healing. That's pretty typical for West Nile virus. In more severe cases, we can see retinal vasculitis and ischemia. So we can see intraretinal hemorrhages, which are a sign of ischemia, definitely vasculitis, and even a neuro-rhetonitis have been described. So West Nile virus is a Flavivirus. It's a single-stranded, small RNA virus. What we know, so the diagram on your right is sort of what we know from animal models, but basically the virions are transmitted through the bite of a mosquito and picked up. They infect and are also just endocytosed by the local antigen-percenting cells. So tissue-resonant macrophages, Langerhans cells and other antigen-percenting cells, brought to the draining lymph nodes where they actually infect macrophages. The macrophages bring the virus to the spleen, and then it's disseminated through the blood. So the virus has multiple proposed mechanisms of getting into the central nervous system. It can either go sort of as a Trojan horse inside a macrophage, which you can kind of see in the bottom here through the blood-brain barrier, or actually the inflammation alone can cause some blood-brain barrier permeability, and the virus can get in that way. And then the virus can transport through the central nervous system via anterograde and retrograde axonal transmission. So interestingly, we know from culture, in vitro culture, that it replicates in RPE cells and exits the cells by exocytosis, which is significant because it doesn't destroy the cells like herpes virus just causes a total necrosis of the cells that infects. This virus actually gets out of the cell and leaves the cell intact. So some pathophysiology questions. Excuse me. Does the virus enter the eye from the CNS via the optic nerve and the neurofiber layer? Or does the virus enter via a compromised blood retinal barrier and then retrograde transport into the central nervous system? So we saw that it was more associated with diabetes, and it's been associated also with diabetic retinopathy, which involves a compromise of the blood retinal barrier. But potentially the virus itself, as it has been shown in mouse models, could cause an endothelial apathy and this diabetic retinopathy-like picture and get into the, thanks, into the retina through its own breakdown of the blood retinal barrier. So can we learn anything from this patient? So this patient, so just kind of zooming in on the presentation. This patient, we saw these white spots, we saw some changes on the autofluorescence, and if we kind of zoom in looking at OCT to kind of find out what's involved, this area doesn't really have much going on in autofluorescence, but you see some subtle changes at the level of the RPE. And this other lesion, we also see some subtle changes at the RPE. So then a week later, dramatic increase in the number of white spots and in the autofluorescence, and also in the disruption of the RPE and overlying outer retina sometimes and the photoreceptor layer. So two weeks later, we kind of can see some consolidation, maybe, of these lesions or some healing. So the lesion shown in OCT on your left, we can see almost like a consolidated RPE hyperfluorescence, maybe a scar, whereas the lesion on the right, although still apparent on autofluorescence, seems to be resolving on OCT. A month later, we kind of see the same picture. We have continued healing of that lesion on the right, where that lesion on the left has sort of still this persistent RPE level defect. And then two months later, it's the same thing. So some of these lesions are involving the RPE, as we know from tissue culture. And some of them are leaving a persistent RPE defect or a scar, and some of them are healing completely or nearly completely. So that's some evidence for RPE involvement. Others have proposed that this is actually an infection that's coming through the retinal neurofiber layer. And the reason they think that is because those lesions seem to not be following the arcades, but actually the neurofiber layer. So that's this group, Karala, they kind of showed this map of the neurofiber layer and that in their patient, the lesion seemed to actually track the neurofiber layer rather than along the arcade. So we actually kind of saw this too, if you recall. We do have lesions along the arcades, but then they're tracking actually along kind of the neurofiber layer path in both eyes. And then if we go recall back to the OCT, we did see neurofiber layer hyper fluorescence, hyperreflectivity, sorry, as well as these RPE changes. So interestingly, interesting, the fact that we see the lesion along a retinal neurofiber layer track but showing up on ICG suggests or tells us that the primary defect, as we saw in OCT, is really not that retinal neurofiber layer but actually the level of the RPE. So possibly the virus is coming in through the neurofiber layer, but the pathology seems to really be, the significant pathology seems to be happening at the level of RPE. So conclusion, stomach observations can be important in elucidating viral pathogenesis. Thanks.