Phosphlipidosis requires intracelllular vesicle {also called lysosomes} formation to become manifest.The vesicles are the hallmark of both phosphlipidosis as well as possible drug resistance.The vesicles normally develop as a part of the manufacture and release of new viruses.
Just to review, Covid, like any virus circulates through the body and infects cells which takes several steps :
1. the viruses attach to cell walls or cell wall receptors ie ACE receptors
2.the viruses enter the cells
3.the viral m protein engages the cellular organelles, Golgi ribosomes etc to manufacture new viruses
4 The mature viruses are encased in vesicles {lysosomes] which attach to the inside of the cell wall and are released into the extracellular spaces where they can infect other cells and complete the process.
"Drug-induced phospholipidosis is a lysosomal storage disorder characterized by an intracellular excessive accumulation of phospholipids {in vesicles}. Its cellular mechanism is still not well understood, but it is known that cationic amphiphilic drugs can induce it. These drugs have a hydrophilic amine head group that can be protonated in the endolysosomal compartment...By compensating the negative surface charge, cationic enzymes are released from the surface of vesicles and proteolytically degraded, triggering a progressive lipid storage and the formation of inactive lamellar bodies...Drug-induced phospholipidosis (DIPL) is caused by long-term treatment of animals and humans with cationic amphiphilic drugs (CADs) leading to an intracellular accumulation of phospholipids in kidney, liver, lung, brain, cornea and other organs."
Reasons it is unlikely Brilacidin could be associated with phosphlipidosis
1 The primary mechanism of action of Brilacidin is killing the virus in the extracellular space.
2. The secondary mechanism of action is Brilacidin prevents viral attachment to the cells.
3 Brilacidin prevents the virus from entering the cell by 2 mechanisms
4. Since it does not enter the cell the phospholipid vesicals or lysosomes will not be formed.
5.A computer modeling study suggested Brilacidin prevents expression of the viral M protein which again would prevent intracellular lysosome formation
6. Phosphlipidosis and Brilacidin drug resistance is prevented by 3 Brilacidin mechanisms of action
7.Phospholipidosis is associated with long term drug usage. Since Brilacidin will only be used 5 days at the most it is not likely to develop a lysosomal storage disorder in a short time period.
"brilacidin exhibits robust inhibition of SARS-CoV-2 in Vero cells and Calu-3 cells, and in two strains of the virus. Likely to function as a viral entry inhibitor [73,74,75], the proposed mechanism of action for brilacidin includes affecting the integrity of the viral membrane and interfering with viral entry."
Remember inherited lysosomal storage disorders in children take years or decades to become manifest.The best known example is Tay-Sachs disease where the young children are normal but they deteriorate with age.