Introduction
Circulating viruses are pathogens that can attach to cells in order to penetrate them further and replicate their copies. Unlike viruses, which live permanently inside cells, circulating viruses are obliged to move around because this is how their mechanism of self-replication works: however, this circulation is the key characteristic that contributes to the functionality of the traps. The article by Zimmer (2007) suggests that traps should be understood as artificially designed or modified cells that contain the same protein receptors that attract viruses in the natural environment.
Discussion
However, unlike normal cells, such traps are devoid of DNA, so a virus trapped in them will not be able to replicate, nor will it be able to escape into the intercellular space. Trapped in an artificial cell, the virus will be forced to die because it lacks the ability to reproduce itself further. The author of the article describes several such examples where cell traps can demonstrate high potential. First, in the fight against HIV, modified red blood cells with CD4 protein receptors could be transfused to a patient with a diagnosis, possibly leading to the retrovirus wanting to bind to such a blood cell but no longer able to escape or replicate. The second, which has already been tested mathematically and practically, is trapping the Coxsackie B virus. CAR protein receptors were created on modified red blood cells that attracted the virus and allowed it to enter the cell, but this was then a dead-end strategy for viral replication. Scientists were able to test the performance of such CAR-modified erythrocytes using mathematical modeling as well as on live rats, which showed reduced virus titer in animal organs as well as higher host survivability.
Susceptibility meets the condition that a cell is capable of serving as a base for viral replication. In theory, any cell that contains DNA can be used by a virus to recreate multiple viral copies through protein synthesis processes. Normal erythrocytes, unlike the modified ones, turn out to be unsusceptible because they do not promote replication, and the latter, unlike the former, is able to attract viruses due to surface protein receptors.
Permissive cells allow viral replication, mainly because the virus can simulate a proper host cell function. Neither normal nor modified erythrocytes can be permissive because they do not possess the DNA that viruses use for replication.
Receptors are to be understood as surface signaling proteins that regulate cell behavior and simultaneously serve as landing sites for beneficial molecules. However, in addition to this, receptors have also been used evolutionarily by viruses as peculiar attachment sites through which the virus can fool the cell’s signaling system and enter. For HIV, the receptors are CD4 proteins located on T cells. For coxsackievirus B, the receptors are CAR proteins.
Whereas host cells have receptors, viruses are coated with ligands that bind to these receptors. In HIV, the ligand is the glycoprotein gp120. The viral ligand of coxsackievirus B is not known for sure and is actually represented not by a single molecule but by a group of them called capsid proteins.
Conclusion
Overall, the findings are encouraging as they demonstrate the effectiveness of viral traps. The lifespan of CAR-modified erythrocyte mice compared to normal mice under conditions of Coxsackie B virus infection increased, and the virus concentration in organ structures decreased. Moreover, computer simulations allowed us to determine that there is a specific limit to the number of such traps, which corresponds to the death of the virus in the organism. On the other hand, to get rid of HIV with such a technology, there are many problems and barriers that need to be solved additionally.
Reference
Zimmer, C. (2007). Scientists explore ways to lure viruses to their death. The New York Times. Web.