We’re currently facing a challenging cold and flu season in Australia. Alongside typical viral culprits like the flu, RSV, and rhinoviruses (which are responsible for the common cold), bacterial pathogens are also significantly affecting health, especially among children. Notable bacterial illnesses include whooping cough and Mycoplasma pneumoniae. Meanwhile, SARS-CoV-2, the virus responsible for COVID-19, is producing recurring waves of infections as it evolves and creates new variants that can sidestep our immune defenses. The most recent variant, referred to as “FLuQE,” is reportedly becoming more prevalent in Australia and other regions. So what should we know about FLuQE?
In the last few months, you might have heard about the “FLiRT” subvariants. These arose from the Omicron variant, JN.1, and include KP.1.1, KP.2, and JN.1.7. KP.2, in particular, played a significant role in COVID-19 cases in Australia and other locations around May. The term FLiRT is derived from specific changes in the spike protein’s amino acids (F456L, V1104L, and R346T). Amino acids are the building blocks of proteins, and the spike protein is crucial for the virus’s attachment to human cells. These modifications arise from mutations, which are random alterations in the virus’s genetic material. The primary aim for SARS-CoV-2 is to develop mutations that enhance the spike protein’s ability to bind to human cell receptors, thus promoting efficient infection (sometimes referred to as viral fitness), while also evading our immune system’s neutralizing antibodies (immune pressure). The FLiRT modifications appear to limit the neutralizing antibodies’ ability to bind to the spike protein, potentially aiding the virus in evading our immunological defenses.
However, the adjustments also seem to affect the virus’s ability to bind to human cells. These conclusions, not yet confirmed through peer-reviewed research, imply that the FLiRT variants might have compromised some of their ability to infect human cells in return for a spike protein that is better at resisting our immune responses. According to experts both in Australia and globally, it seems that an additional mutation in FLuQE may have restored the viral fitness potentially diminished by the FLiRT mutations. The FLuQE variant (KP.3) directly descends from FLiRT, retaining the same mutations as its predecessors, but with an added amino acid alteration in the spike protein, known as Q493E, after which FLuQE is named. This mutation changes a glutamine at position 493 to glutamic acid in the spike protein, which is 1,273 amino acids long.
While glutamine is a neutral amino acid, glutamic acid carries a negative charge, altering the spike protein’s properties, which could enhance the virus’s ability to enter human cells. It’s still early concerning FLuQE, and more research is required. Yet, it seems we are dealing with another immune-evasive virus that remains highly capable of infecting our cells, which explains why FLuQE is becoming more prevalent in various countries. With the extensive spread of the FLiRT and FLuQE variants, community immunity will gradually develop, and over time, these variants’ dominance will be surpassed by another immune-evasive version. The competition between our immune defenses and the evolution of SARS-CoV-2 is ongoing. Currently, the problem we face is that vaccines do not fully prevent infection or hinder virus spread. While vaccines effectively guard against serious illness, the virus still infects a significant number of people. This results in a burden on individuals and healthcare systems and provides more chances for the virus to evolve. The more opportunities the virus has to mutate in a way that helps it bypass our immune system and infect our cells, the more likely it will achieve this.
Next-gen vaccines and treatments are essential to strengthen immunity in the upper respiratory system (the nose and throat) to decrease infections and transmissions, as this is where the virus first establishes an infection. A human challenge study, where volunteers are deliberately exposed to SARS-CoV-2, indicated that those who did not get infected had a strong antiviral immune response in their upper respiratory tract. Therefore, immune-boosting nasal sprays and nasal vaccines are under clinical development. It is hoped that this approach will help slow the evolution of SARS-CoV-2 and the development of new subvariants that continue to cause waves of infections and disease.