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The basket‐weave pattern is present in the skin for a reason

HHV-6 PCRs were performed. The majority of the viral cohort were defined by positive HHV-6 PCR (11 of 18) and positive HHV-6 IgG (10 of 18; IgM testing was not performed). The combined viraland drug-induced group had similar results (5 of 5 and 4 of 5 positive PCR and positive IgG, respectively). Representative members of each subgroup were subsequently analysed by shotgun metagenomics and cytokine profiling. Interestingly, metagenomics analysis of skin and blood samples failed to confirm the presumed aetiological virus in all four patients in the viral group. In fact, in one patient in whom parvovirus B19 had been implicated, metagenomics and a posteriori PCR testing revealed enterovirus A to be the viral culprit. Another patient in the drug-induced cohort also had positive metagenomics testing for enterovirus A. These findings question the utility of serum-derived serologies and PCRs in identifying viral triggers of cutaneous reactions. However, it is possible that serum testing for other common viral causes of AE, including picornaviruses, adenovirus and HHV7, could bridge this diagnostic gap. Additionally, high IgG titres were cited as evidence of HHV-6 reactivation resulting in AE during the initial patient stratification; however, without convalescent immunoglobulin titres to demonstrate fourfold increase, the validity of this assumption is unclear. The high sensitivity of HHV-6 PCR, as the authors allude to, makes differentiation between primary, reactivated and latent infection difficult. Thus, there may be a risk of misclassification bias in this study and in real-world utilization of HHV-6 testing in the dermatological setting. Clinicians should exercise caution when attributing AE to HHV-6 reactivation. Similar unexpected results were found in the cytokine analysis. As the authors point out, a T helper 1 response would be expected in viral AEs. However, consistent differences in cytokine profiles were not demonstrated between the patient groups. Whether this is due to misclassification bias or other influences is unclear. While specific molecular features distinguishing viralfrom drug-induced AE remain elusive, this study highlights the potential for metagenomics in identifying previously underrecognized aetiologies of AE. Future efforts might refine patient stratification with the addition of picornavirus, adenovirus and HHV-7 testing, convalescent HHV-6 titres and drug rechallenge to discover whether metagenomics and cytokine profiling continue to challenge our current diagnostic armamentarium, and how novel molecular methods might offer new insights into the differentiation of AE.