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Clues to Long COVID Linked to Virulence and Infectivity Found in Shell Proteins
Gerard Kian-Meng Goh1, James A Foster2,3, Vladimir N Uversky4
1Goh's BioComputing, Singapore 548957, Singapore.
Advances in Respiratory Medicine
|March 24, 2026
Summary
The shell disorder of SARS-CoV-2, the virus causing COVID-19, influences its infectivity and virulence. This shell disorder model explains how the virus evades immune responses and potentially causes long COVID.
Area of Science:
- Virology
- Computational Biology
- Immunology
Background:
- COVID-19 (caused by SARS-CoV-2) exhibits distinct virulence and infectivity compared to SARS-CoV-1.
- Viral shell structure is increasingly recognized as a factor in pathogen-host interactions.
Purpose of the Study:
- To investigate the role of viral shell disorder in SARS-CoV-2 infectivity and virulence.
- To explore the potential of shell disorder models (SDMs) in explaining COVID-19 pathogenesis, including long COVID.
Main Methods:
- Utilized an AI disorder-predicting tool to analyze the structural disorder of SARS-CoV-2 and SARS-CoV-1 outer (M) and inner (N) shells.
- Compared shell disorder patterns between SARS-CoV-2 and SARS-CoV-1.
- Examined the link between shell disorder and viral infectivity, virulence, and potential immune evasion mechanisms.
Main Results:
- SARS-CoV-2 possesses an unusually hard (low disorder) outer shell (M) compared to SARS-CoV-1, potentially enhancing resistance to antimicrobial enzymes and increasing shedding.
- The inner shell (N) of SARS-CoV-2 shows lower disorder than SARS-CoV-1, correlating with lower virulence.
- The hard M shell may also resist immunological enzymes, allowing macrophages to become viral reservoirs.
Conclusions:
- Shell disorder models (SDMs) provide a coherent framework for understanding SARS-CoV-2 infectivity, virulence, and potentially long COVID.
- The structural properties of the SARS-CoV-2 shell are critical determinants of its biological behavior and interaction with the host immune system.
Keywords:
AICOVID-19NL63Omicronartificial intelligenceattenuationcomplement systemcontagiousnesscoronavirusdendritichard shellimmuneinfectivityintrinsic disorderlong COVIDlysosomemacrophagemembranemonocyteneutrophilnucleocapsidnucleoproteinpangolinpathogenesisperforinphagocytephagocytosisreservoirshellspikeunstructuredvariantvirulence
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