As of 7 th July, 2020, more than 11,700,000 people worldwide have been confirmed to get COVID-19(Velavan et al., 2020) . The rapid pandemic has posed serious threats to physical and mental health of people all around the world. Posttraumatic stress disorder (PTSD) is a post-traumatic event that occurs during unbearable experience, such as torture, accident, violent assault or natural disaster, which was manifested as persistent trauma, evasion of related stimuli, emotional indifference and physiological irritability (Eurosurveillance et al., 2020) . The prevalence of PTSD in trauma survivors is 7-12% (Deja et al., 2006) . During SARS occurred in 2003, approximately 10% of people developed symptoms of PTSD and nearly 20% patients got PTSD during Ebola virus outbreak in West Africa (Koenen et al., 2017) . The COVID-19 pandemic could be recognized as a bio-disaster followed by a psychological impact.
Going through COVID-19 could be a traumatic experience. PTSD would develop into long-term psychiatric disorders among survivors of COVID-19 without timely intervention. Unlike the commonly described PTSD, PTSD caused by biological disasters might be complicated and chronic (Banerjee and Viswanath, 2020) . With the J o u r n a l P r e -p r o o f increasing global burden of the SARS-CoV-2 during this pandemic, preliminary data on COVID-19 related PTSD have been reported. It is necessary to discuss and review the current data on high prevalence of PTSD and its potential mechanisms, and measures should be timely taken to prevent the occurrence and development of PTSD (Tandon, 2020) .
other organs or tissues. Peripheral inflammatory cytokines could affect the brain through various mechanisms. The common pathway includes active transport through blood-brain barrier (BBB), leaky area of BBB, activation of vagal nerve or other neural pathways. Therefore, the peripheral inflammation caused by COVID-19 can lead to neuroinflammation by activating astrocytes and microglia ( Figure 1 ).
Particularly, IL-1β, TNF-α and IL-6 plays potential role in the synaptic plasticity, neurogenesis, and memory/learning from the morphological, functional and cognitive levels, presenting with PTSD symptoms. Another mechanism of widespread concern is that proinflammatory cytokines induced by COVID-19 upregulate indoleamine 2,3dioxygenase, which was the initial and speed-limiting enzyme of tryptophan degradation pathway (i.e., kynurenine pathway). The activation of indoleamine 2,3-