Health Viewpoints
The new JN.1 variant of COVID-19 has been spreading rapidly around the world.JN.1 was first detected in August. It has since been identified in 12 countries, including the United States.

JN.1 Has Tricks
JN.1 originates from a subvariant of Omicron “Pirola”—BA.2.86 and is a recombinant form of two variants: the early BA.2 sublineage and the subsequent XBB lineage.What’s particularly concerning about JN.1 is its notable divergence from other recently prevalent variants.
Weakened Protection by XBB.1.5 Vaccine
An October preprint paper by Dr. Yunlong Cao from Peking University also showed the XBB variants’ mutations at sites 455 and 456 that help these viruses further avoid the body’s immunity, especially neutralizing antibodies.In simpler terms, the virus adapts, making it harder for our immune system to fight it off, even if people have been vaccinated or had previous COVID-19 infections.
Notably, JN.1 contains a new mutation of L455S, making the latest XBB.1.5 vaccine less likely to protect against JN.1.
Increased Immune Escape Potential
When our immune system fights a virus, it’s like a complete battle involving various types of immune cells and mechanisms.Each cell has its method of efficiently recognizing and eliminating the virus. This recognition process is based on unique virus parts identified by each cell type.
To picture this, think of your hand with five fingers. When you wear gloves, each finger goes into a specific part of the glove. Similarly, when a virus enters our body, each immune cell identifies a distinct part of its surface and attacks it differently.
If a virus’ spike protein mutates, the antibodies produced by significant immune cells—B-cells may not be able to fight against the mutated virus effectively. On the other hand, if a virus mutates in the non-spike protein, another primary type of immune cell—T-cells, may be unable to protect against the variant.
In the case of JN.1, changes in the spike protein contribute to its increased infectivity and escape from vaccine or infection-induced neutralizing antibodies.
In summary, mutations in the more viral proteins could enhance the virus’s ability to escape from established immunity and cause disease, potentially making infections more severe.
Although the authors remain optimistic about the potential protection of the XBB vaccine against Pirola, the virus has already learned to escape from the vaccine-induced or previous infection-induced T-cell immunity on top of B-cell immunity.
White Lung Syndrome in China and the US
Even though direct data does not indicate a more severe disease, there is a specific concern about JN.1.Along with the rise of JN.1, a mysterious disease has also appeared.
Since late November, a surge of thousands of mysterious pneumonia cases has flooded into the hospitals of Beijing, Tianjin, and Shanghai. The large number of patients and severity of cases have raised an alarm similar to China’s initial January 2020 COVID-19 outbreak.
The symptoms of “white lung syndrome” (a folk name for severe pneumonia) include high fevers and unusual symptoms of silent hypoxia that are similar to COVID-19-associated pneumonia.
Reported cases in children with “white lung pneumonia” or “white lung syndrome” in the United States and Europe are escalating, increasing public concern alongside the rising JN.1 curve.
The onset of this mysterious pneumonia in August occurred in the same month that JN.1 was detected. Nothing is coincidental.
Although a medical analysis of the pathogen of this pneumonia is lacking, there are several red flags when we attribute these lung problems to mycoplasma.
The SARS-CoV-2 virus and mycoplasma are completely different pathogens, yet the symptoms of pneumonia caused by both appear to be similar—they attack different parts of the lung with different clinical courses.
The human lungs exhibit a structure extending from the larger trachea to smaller units like alveoli, supported by the interstitium between these alveoli.
SARS-CoV-2 gains entry through ACE2 receptors, which are distributed abundantly in alveolar cells, leading to pneumonia and marked by damage to both alveoli and the interstitium. Severe cases are evident as “large white lungs” on X-rays, signifying widespread inflammation.
In contrast, mycoplasma affects the bronchi, causing milder inflammation, usually without severe pneumonia. It is generally mild and improves in about one week.
Media reports on severe white lung cases resembling prolonged COVID-19 progression raise concerns.
China does not routinely test for the SARS-CoV-2 virus in patients with pneumonia; the actual number of JN.1 strains in China is unknown.
Many countries have relaxed their COVID-19 RNA testing protocols, particularly in cases involving children. The challenge arises when individuals, especially those with pneumonia symptoms, may not immediately consider undergoing a COVID-19 test. Without conducting a COVID-19 test, it becomes less likely to determine whether the JN.1 variant causes the infection.
This situation is prone to underestimating the prevalence of JN.1 cases outside of China. Moreover, within China, the problem of concealed cases and non-transparent reporting significantly skews the count of potential JN.1 cases. These issues contribute to a systemic underestimation of JN.1 cases within China.
Even though we do not have adequate case data to help us make better judgments about the link between these two “coincidental” phenomena this winter, the overlapping timing with a more complex mutation, more aggressive immune escape, and the potential increase in severity may all contribute to the possible link between them. This warrants a deeper medical and laboratory investigation of the current pneumonia cases, including SARS-CoV-2 gene sequencing.
Future Reflections
People may argue that vaccines help reduce the death rate, but a new study may change this notion.Government officials have yet to find effective measures to control the remaining COVID-19 surges.
The virus has proven resilient, mutating to counteract our vaccines. The critical question remains: How are we going to bring an end to this ongoing pandemic? Without understanding how to eradicate the virus at its core, it will merely persist in playing a cat-and-mouse game with humanity.
To address this unprecedented challenge, it’s essential to revisit the question of the SARS-CoV-2 origin. Only by identifying the root cause can we effectively and swiftly resolve this issue.