There do seem to be some alternative views on the role of this protein, LRRC15, in the lungs with respect to Sars-CoV-2. See this other paper (Feb 3 2023):
https://journals.plos.org/plosbiology/article?id=10.1371/jou...
Just to cover the basics, the virus normally accesses cells by binding to ACE2.
> "The interactions between Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) and human host factors enable the virus to propagate infections that lead to Coronavirus Disease 2019 (COVID-19). The spike protein is the largest structural component of the virus and mediates interactions essential for infection, including with the primary angiotensin-converting enzyme 2 (ACE2) receptor."
There is a key role played in viral production by furin in ACE2-receptor-binding, which is an 'ubiquitous serine protease' in mammalian cells which plays key roles in processing hormones, growth factors, etc. and which is also exploited by many infectious diseases. This feature of Sars-CoV-2 is of course directly related to the notion that the virus was engineered, because:
> "The presence of a multibasic site (Arg-Arg-Ala-Arg) located at the S1–S2 junction, which is cleaved by furin (Fig. 1), distinguishes SARS-CoV-2 from SARS-CoV and all other known sarbecoviruses whose S protein is not cleaved by furin-like proteases during virus maturation in the infected cell. Cleavage of the S1–S2 boundary is a prerequisite for the cleavage of the S2′ site126, and both cleavage events are essential to initiate the membrane-fusion process."
https://www.nature.com/articles/s41580-021-00418-x
Accounting for the appearance of this furin cleavage site is a problem for anyone promoting a 'natural origin theory'.
Getting back to this new protein and its potential role, the other paper (first source above) seems to have a different conclusion:
> "Levels of LRRC15 were greatly elevated by inflammatory signals in the lungs of COVID-19 patients. Although infection assays demonstrated that LRRC15 alone is not sufficient to permit viral entry, we present evidence that it can modulate infection of human cells. This unexpected interaction merits further investigation to determine how SARS-CoV-2 exploits host LRRC15 and whether it could account for any of the distinctive features of COVID-19."
Their work seems to imply it might not block infection of cells, but instead enhance infection:
> "In order to examine whether LRRC15 might modulate the efficiency of viral entry into ACE2-expressing cells, we employed the naturally susceptible human lung cell line (CaLu-3) that is commonly used as a model for coronavirus infection [47]. We introduced LRRC15 ectopically to these cells to emulate the expression seen in other human lung cell populations we identified in our expression analysis. Compared to unmodified CaLu-3 cells that lack any detectable LRRC15, the expression of LRRC15 modestly enhanced viral infection"
Science is complicated, and popular media reports on recent science are often of very poor quality.