The novel coronavirus disease is a pandemic with high fatality rate, especially in the elderly population and patient groups with comorbidities such as hypertension, cardiovascular disease, chronic kidney failure, and cancer (3). As of May 1, 2020, the fatality rate of the infection was determined as 1.4% (4). The transmissibility of a virus is indicated by its reproductive number (Ro), which shows how fast the virus spreads. Ro was determined to be 3.77 according to clinical and epidemiological data from 8866 patients in 30 provinces, a value higher than the Ro of the severe acute respiratory virus (Ro: 2–3) (6). For this reason, it is difficult to control the pandemic, despite isolation preventions.
Prolonged viral shedding and the possibility of reinfection in some people are other problems that make pandemic management difficult. Virus RNA was reported to have been isolated from the sputum and feces of patients a few weeks after their discharge (8). Another study from Wuhan reported that the virus was detected for a median of 20 days (up to 37 days among survivors) after symptom onset (13). In our case, three months between two infections excludes the possibility of prolonged viral shedding.
Although the causes of COVID-19 reinfection are not yet fully clarified, the number of reported cases is increasing. Reinfection is defined as the detection of SARS-CoV-2 PCR positivity again after two PCR tests taken every 24 hours are negative. Theoretically, the SARS-CoV-2 genome must be the same in both infections. Evidence suggests that possible causes of reinfection include short-lived protective immunity and re-exposure to genetically different forms of the same viral strain (12). Another reason can be cross-contamination from another betacoronavirus, but as in our case, COVID-compatible tomography findings support COVID-19 reinfection (14). Sequencing and phylogenetic analysis of the SARS-CoV-2 genome in reinfection cases may be useful for understanding viral pathogenesis.
The antibody response in patients with COVID-19 remains largely unknown. For the majority of individuals infected with SARS-CoV-2, neutralizing immunoglobulin (IgM and IgG) levels rise within days to weeks of symptom onset (10). Many human infections with other viral pathogens, such as the influenza virus, do not produce a durable immune response. The durability of IgG against SARS-CoV-2 has yet to be defined; persistence up to 40 days from symptom onset has been reported (11). In our patient, reinfection was expected because the antibody response was not as effective due to the splenectomy. On the other hand, positive RNA tests have been reported despite seropositivity for IgG after the primary infection (9). Jianghong et al. also showed that patients who were admitted to the hospital due to reinfection had the second disease with mild symptoms regardless of the antibody response (15). However, in our patient, extensive lung involvement and severe symptoms developed in the second attack.
Although the detection of antibody levels is important for herd immunity and epidemiological data, natural killer and CD 8+ T cells are the first defense mechanisms against all viral infections. In the absence of protective antibodies (in case of a splenectomy), it is possible that protective mechanisms through other arms of the immune response (memory and cytotoxic T cells) alter the course of the COVID-19 disease upon reinfection (16). Memory T cells have been shown to serve a very important role in the long-term protection against infection from SARS-CoV-2 infection, which is a member of the family Coronaviridae (17).
An antibody test was not performed on our patient because it was thought that there was no effective antibody due to the splenectomy. In this case, reinfection could be explained by a decrease in the amount of memory T cells or the loss of function. Bo et al. demonstrated a drop in T lymphocyte subgroup count in severely ill patients, including deceased patients (18). Zhang et al. also noted that this reduction could be explained by the atrophy of the spleen and lymph node, thereby highlighting the role of SARS-CoV-2 in potentiating cell degeneration (19).
In conclusion, unlike most common cold viruses, immunity to SARS-CoV-2 involves both cell-mediated and humoral responses. Reinfection in a splenectomy case may help researchers understand the pathogenesis of the disease and can be a guide for the development of vaccines and new treatments.