In Reply Yu and Freund propose that the conflicting clinical and histological observations in PORN could be explained by retinal whitening from vascular occlusion of deep retinal capillaries, a process that immediately precedes inner retina injury followed by photoreceptor involvement. They base this hypothesis on recent observations by Sarraf et al,1 who used high-resolution spectral-domain OCT in paracentral acute middle maculopathy. Previous studies describing OCT findings in patients with PORN, however, were done with time-domain OCT, so details of specific layers of affected retina were not discernible. Having the proposed mechanism of Yu and Freund in mind, we reviewed the remaining slides from the case of PORN that showed partial-thickness necrosis, specifically looking for evidence of retinal microvascular disease. At this stage of the infection, no small retinal capillaries could be found on hematoxylin-eosin–stained sections; only larger-diameter vessels in the inner retina were found. These vessels did not appear occluded. Not mentioned in our earlier article2 was the disproportionately larger number of intranuclear inclusions (viral inclusions) in the inner nuclear layer compared with the outer nuclear layer (Figure). Almost all nuclei of the inner nuclear layer contained red inclusion bodies, while viral inclusions were found substantially less often in nuclei of photoreceptors (Figure, inset). From a solely morphological perspective, the infection appears to spread contiguously. This, however, does not adequately explain the early clinical appearance of deep retinal whitening when more advanced involvement appears in the inner retina histologically. We suspect such riddles will eventually be solved through the use of new technologies and thoughtful analysis like that presented by Yu and Freund.