Faculty of Medicine, School of Psychiatry, University of New South Wales, Sydney, NSW, 2052, Australia.
South Western Sydney Area Health Service, Sydney, NSW, 2170, Australia.
Transl Psychiatry. 2021 Mar 15;11(1):160. doi: 10.1038/s41398-020-01151-3.
Psychiatric symptoms are seen in some COVID-19 patients, as direct or indirect sequelae, but it is unclear whether SARS-CoV-2 infection interacts with underlying neuronal or psychiatric susceptibilities. Such interactions might arise from COVID-19 immune responses, from infection of neurons themselves or may reflect social-psychological causes. To clarify this we sought the key gene expression pathways altered in COVID-19 also affected in bipolar disorder, post-traumatic stress disorder (PTSD) and schizophrenia, since this may identify pathways of interaction that could be treatment targets. We performed large scale comparisons of whole transcriptome data and immune factor transcript data in peripheral blood mononuclear cells (PBMC) from COVID-19 patients and patients with psychiatric disorders. We also analysed genome-wide association study (GWAS) data for symptomatic COVID-19 patients, comparing GWAS and whole-genome sequence data from patients with bipolar disorder, PTSD and schizophrenia patients. These studies revealed altered signalling and ontology pathways shared by COVID-19 patients and the three psychiatric disorders. Finally, co-expression and network analyses identified gene clusters common to the conditions. COVID-19 patients had peripheral blood immune system profiles that overlapped with those of patients with psychiatric conditions. From the pathways identified, PTSD profiles were the most highly correlated with COVID-19, perhaps consistent with stress-immune system interactions seen in PTSD. We also revealed common inflammatory pathways that may exacerbate psychiatric disorders, which may support the usage of anti-inflammatory medications in these patients. It also highlights the potential clinical application of multi-level dataset studies in difficult-to-treat psychiatric disorders in this COVID-19 pandemic.
一些 COVID-19 患者出现了精神症状,无论是直接的还是间接的后遗症,但尚不清楚 SARS-CoV-2 感染是否与潜在的神经元或精神易感性相互作用。这种相互作用可能来自 COVID-19 的免疫反应,来自神经元本身的感染,或者可能反映了社会心理原因。为了阐明这一点,我们寻求了在 COVID-19 中改变的关键基因表达途径,这些途径也在双相情感障碍、创伤后应激障碍(PTSD)和精神分裂症中受到影响,因为这可能确定了可以作为治疗靶点的相互作用途径。我们对 COVID-19 患者和精神障碍患者的外周血单核细胞(PBMC)中的全转录组数据和免疫因子转录数据进行了大规模比较。我们还分析了有症状 COVID-19 患者的全基因组关联研究(GWAS)数据,将 GWAS 数据与双相情感障碍、PTSD 和精神分裂症患者的全基因组序列数据进行了比较。这些研究揭示了 COVID-19 患者和三种精神障碍患者共有的改变的信号和本体途径。最后,共表达和网络分析确定了与这些疾病共同的基因簇。COVID-19 患者的外周血免疫系统特征与精神障碍患者的特征重叠。从确定的途径来看,PTSD 特征与 COVID-19 的相关性最高,这也许与 PTSD 中看到的应激-免疫系统相互作用一致。我们还揭示了可能加重精神障碍的共同炎症途径,这可能支持在这些患者中使用抗炎药物。这也突出了在 COVID-19 大流行期间,对难以治疗的精神障碍进行多层面数据集研究的潜在临床应用。