Research

Researches

02 Nov 2020

COVID-19: Persons Without A Robust Neutralizing Antibody Response Might Be At Risk For SARS-COV-2 Reinfection

Asmaa Hachim and Niloufar Kavian from Sophie Valkenburg's team have published in Emerging Infectious Diseases about reinfection and serologic responses in healthy adult with SARS-CoV-2. Emerging Infectious Diseases, an open access, peer reviewed journal published monthly by the Centers for Disease Control and Prevention, promotes the recognition of new and reemerging infectious diseases around the world and improves the understanding of factors involved in disease emergence, prevention, and elimination.

Details:
Whether SARS-CoV-2 infection induces serologic immunity and the duration of that immunity is unknown. In humans, reinfection with seasonal coronaviruses occurs naturally and in experimental conditions. The group worked on the first SARS-CoV-2 re-infection case that was described world-wide, and that was detected in Hong Kong.
 
In March 2020, a healthy 33-year-old man developed mild signs and symptoms of COVID-19, and was confirmed with a new SARS-CoV-2 infection later in August without symptoms. Their findings show that the first infection did not triggered virus neutralizing antibodies, and that, in the absence of primary neutralizing antibodies, T cells and mucosal immunity might have played a critical role in resolving the infection.
 
Previous studies show that most patients with mild, severe, or asymptomatic SARS-CoV-2 infection produce neutralizing antibodies and antibodies against spike RBD and N proteins. This case was unusual because the patient had low or undetectable levels of neutralizing and binding antibodies against multiple viral proteins during his primary infection and acute stage of asymptomatic reinfection. He was not immunodeficient because he had IgG against measles and varicella zoster viruses and no history of recurrent infections. The virus from the first infection had a truncation in the 58AA open reading frame 8 gene, which mediates immune evasion through downregulation of major histocompatibility complex and interferon responses. However, it is unclear if this mutation contributed to the patient’s lack of antibody production.
 
Reasons for this patient’s unusual response need to be further investigated. He recovered from his primary infection within 3 weeks, and his secondary infection was asymptomatic. These findings indicate that, in the absence of primary neutralizing antibodies, T cells and mucosal immunity might have played a critical role in resolving the infection. Given the unusual antibody response in this patient to his first infection, researchers must be cautious about generalizing more widely from this patient’s experience.