Reinfection with two genetically distinct SARS-CoV-2 viruses within 19 days.
Ontology highlight
ABSTRACT:
SUBMITTER: Tang CY
PROVIDER: S-EPMC8426799 | biostudies-literature |
REPOSITORIES: biostudies-literature
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| S-EPMC8242781 | biostudies-literature
Project description:From February 26, 2020 to March 11, 2021, coronavirus disease 2019 (COVID-19) pandemic resulted in 11,439,558 cases and 277,102 deaths in Brazil. Among them, 2,195,130 cases and 63,965 deaths occurred in Sao Paulo State, Southeast Brazil. The recent emergence and rise of new variants of SARS-CoV-2 is of concern because of their higher transmissibility and possible association with more severe disease. Cases of SARS-CoV-2 reinfections have been described since December 2020 in Brazil. This report describes two cases of COVID-19 reinfection, that occurred five and six months after the first infection, during the second wave of the pandemic in Sao Paulo State. Both patients presented mild symptoms in the two COVID-19 episodes and different lineages of SARS-CoV-2 were identified: B.1.1.33 and B.1.1.28 lineages in case 1 and B1.1.128 and P. 2 lineages in case 2.
| S-EPMC8216690 | biostudies-literature
Project description:ObjectivesTo date, reported SARS-CoV-2 reinfection cases are mainly from strains belonging to different clades. As the pandemic advances, a few lineages have become dominant in certain areas leading to reinfections by similar strains. Here, we report a reinfection case within the same clade of the initial infection in a symptomatic 28-year-old-male in Quito-Ecuador.MethodsInfection was detected by reverse transcription-polymerase chain reaction, and immune response evaluated by antibody testing. Whole-genome sequencing was performed and phylogenetic analysis conducted to determine relatedness.ResultsBoth the infection and the reinfection strains were assigned as Nextstrain 20B, Pangolin lineage B.1.1 and GISAID clade O. Our analysis indicated 4-6 fold more nucleotide changes than are expected for reactivation or persistence compared with the natural rate of SARS-CoV-2 mutation (∼2-3 nucleotide changes per month), thus supporting reinfection. Furthermore, approximately 3 months after the second infection, COVID-19 antibodies were not detectable in the patient, suggesting potential vulnerability to a third infection.ConclusionsOur results showed evidence of SARS-CoV-2 reinfection within the same clade in Ecuador, indicating that previous exposure to SARS-CoV-2 does not guarantee immunity in all cases.
| S-EPMC8078048 | biostudies-literature
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| S-EPMC8099311 | biostudies-literature
Project description:Infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has become pandemic and the duration of protective immunity to the virus is unknown. Cases of persons reinfected with the virus are being reported with increasing frequency. At present it is unclear how common reinfection with SARS-CoV-2 is and how long serum antibodies and virus-specific T cells persist after infection. For many other respiratory virus infections, including influenza and the seasonal coronaviruses that cause colds, serum antibodies persist for only months to a few years and reinfections are very common. Here we review what is known about the duration of immunity and reinfection with coronaviruses, including SARS-CoV-2, as well as the duration of immunity to other viruses and virus vaccines. These findings have implications for the need of continued protective measures and for vaccines for persons previously infected with SARS-CoV-2.
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Project description:ACE2 on epithelial cells is the SARS-CoV-2 entry receptor. Single-cell RNA-sequencing data derived from two COVID-19 cohorts revealed that MAP4K3/GLK-positive epithelial cells were increased in patients. SARS-CoV-2-induced GLK overexpression in epithelial cells correlated with COVID-19 severity and vesicle secretion. GLK overexpression induced the epithelial cell-derived exosomes containing ACE2; the GLK-induced exosomes transported ACE2 proteins to recipient cells, facilitating pseudovirus infection. Consistently, ACE2 proteins were increased in the serum exosomes from another COVID-19 cohort. Remarkably, SARS-CoV-2 spike protein stimulated GLK, and GLK stabilized ACE2 in epithelial cells. Mechanistically, GLK phosphorylated ACE2 at two serine residues (Ser776, Ser783), leading to dissociation of ACE2 from its E3 ligase UBR4. Reduction of UBR4-induced Lys48-linked ubiquitination at three lysine residues (Lys26, Lys112, Lys114) of ACE2 prevented its degradation. Furthermore, SARS-CoV-2 pseudovirus or live virus infection in humanized ACE2 mice induced GLK and ACE2 protein levels, as well as ACE2-containing exosomes. Collectively, ACE2 stabilization by SARS-CoV-2-induced MAP4K3/GLK may contribute to the pathogenesis of COVID-19.
| S-SCDT-EMM-2022-15904 | biostudies-other
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| S-EPMC7833993 | biostudies-literature
Project description:A healthcare worker presented with fever, cough, headache and tested positive by SARS-CoV-2 real time reverse transcriptase polymerase chain reaction (qRT-PCR). He got admitted to hospital and recovered after 14 days. After 2 months, as a screening protocol considering the high risk setup he got tested and again found to be positive for SARS-CoV-2 by qRT-PCR. Our patient had detectable levels of Anti-SARS-CoV-2 IgG antibodies during the reinfection but found negative for Neutralizing antibodies (NAb). Our findings suggest that the person after the initial infection might not develop the desired protective immunity to prevent the reinfection as demonstrated by absence of NAb.
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