Editing Antiviral drug (section)

====Before cell entry====
One antiviral strategy is to interfere with the ability of a virus to infiltrate a target cell. The virus must go through a sequence of steps to do this, beginning with binding to a specific "[[receptor (biology)|receptor]]" molecule on the surface of the host cell and ending with the virus "uncoating" inside the cell and releasing its contents. Viruses that have a lipid envelope must also fuse their envelope with the target cell, or with a vesicle that transports them into the cell before they can uncoat.

This stage of viral replication can be inhibited in two ways:
# Using agents which mimic the virus-associated protein (VAP) and bind to the cellular receptors. This may include VAP [[anti-idiotypic]] antibodies, natural [[ligand]]s of the receptor, and anti-receptor antibodies.
# Using agents which mimic the cellular receptor and bind to the VAP. This includes anti-VAP [[antibody|antibodies]], receptor anti-idiotypic antibodies, extraneous receptor and synthetic receptor mimics.

This strategy of designing drugs can be very expensive, and since the process of generating anti-idiotypic antibodies is partly trial and error, it can be a relatively slow process until an adequate molecule is produced.

=====Entry inhibitor=====
{{Main|Entry inhibitor}}
A very early stage of viral infection is [[viral entry]], when the virus attaches to and enters the host cell. A number of "entry-inhibiting" or "entry-blocking" drugs are being developed to fight HIV. HIV most heavily targets a specific type of lymphocyte known as "helper T cells", and identifies these target cells through T-cell surface receptors designated "[[CD4]]" and "[[CCR5]]". Attempts to interfere with the binding of HIV with the CD4 receptor have failed to stop HIV from infecting helper T cells, but research continues on trying to interfere with the binding of HIV to the CCR5 receptor in hopes that it will be more effective.

HIV infects a cell through fusion with the cell membrane, which requires two different cellular molecular participants, CD4 and a chemokine receptor (differing depending on the cell type). Approaches to blocking this virus/cell fusion have shown some promise in preventing entry of the virus into a cell. At least one of these entry inhibitors—a biomimetic peptide called [[Enfuvirtide]], or the brand name Fuzeon—has received FDA approval and has been in use for some time. Potentially, one of the benefits from the use of an effective entry-blocking or entry-inhibiting agent is that it potentially may not only prevent the spread of the virus within an infected individual but also the spread from an infected to an uninfected individual.

One possible advantage of the therapeutic approach of blocking viral entry (as opposed to the currently dominant approach of viral enzyme inhibition) is that it may prove more difficult for the virus to develop resistance to this therapy than for the virus to mutate or evolve its enzymatic protocols.

=====Uncoating inhibitors=====
Inhibitors of uncoating have also been investigated.<ref name="pmid10325536">{{cite journal |author=Bishop NE |title=Examination of potential inhibitors of hepatitis A virus uncoating |journal=Intervirology |volume=41 |issue=6 |pages=261–71 |year=1998 |pmid=10325536 |doi= 10.1159/000024948|s2cid=21222121 }}</ref><ref name="pmid1850030">{{cite journal |vauthors=Almela MJ, González ME, Carrasco L |title=Inhibitors of poliovirus uncoating efficiently block the early membrane permeabilization induced by virus particles |journal=J. Virol. |volume=65 |issue=5 |pages=2572–77 |date=May 1991 |pmid=1850030 |pmc=240614|doi=10.1128/JVI.65.5.2572-2577.1991 }}</ref>

[[Amantadine]] and [[rimantadine]] have been introduced to combat influenza. These agents act on penetration and uncoating.<ref name="isbn0-7817-4673-6">{{cite book |author1=Beringer, Paul |author2=Troy, David A. |author3=Remington, Joseph P. |title=Remington, the science and practice of pharmacy |publisher=Lippincott Williams & Wilkins |location=Hagerstwon, MD |year=2006 |page=1419 |isbn=978-0-7817-4673-1}}</ref>

[[Pleconaril]] works against [[rhinovirus]]es, which cause the [[common cold]], by blocking a pocket on the surface of the virus that controls the uncoating process. This pocket is similar in most strains of rhinoviruses and [[enterovirus]]es, which can cause diarrhea, [[meningitis]], [[conjunctivitis]], and [[encephalitis]].<ref>{{cite journal |title=Activity of Pleconaril against Enteroviruses |author1=Daniel C. Pevear |author2=Tina M. Tull |author3= Martin E. Seipel |journal=Antimicrobial Agents and Chemotherapy |year=1999|volume=43 |issue=9 |pages=2109–2115 |doi=10.1128/AAC.43.9.2109 |pmid=10471549 |pmc=89431 }}</ref>

Some scientists are making the case that a vaccine against rhinoviruses, the predominant cause of the common cold, is achievable.
Vaccines that combine dozens of varieties of rhinovirus at once are effective in stimulating antiviral antibodies in mice and monkeys, researchers reported in ''[[Nature Communications]]'' in 2016.<ref>{{cite news |url=https://www.nature.com/articles/ncomms12838 |author1=Lee, S. |author2=Nguyen, M. |author3=Currier, M. |title=A polyvalent inactivated rhinovirus vaccine is broadly immunogenic in rhesus macaques |publisher=Nature Communications |year=2016}}</ref>

Rhinoviruses are the most common cause of the common cold; other viruses such as [[respiratory syncytial virus]], [[parainfluenza virus]] and [[adenoviruses]] can cause them too.<ref>{{cite web |url=https://bready.blog.ranftl.org/health/common-cold-causes |title=Common Cold Causes: Rhinoviruses and More |access-date=8 January 2022 |archive-date=8 January 2022 |archive-url=https://web.archive.org/web/20220108160711/https://bready.blog.ranftl.org/health/common-cold-causes |url-status=dead }}</ref> Rhinoviruses also exacerbate asthma attacks. Although rhinoviruses come in many varieties, they do not drift to the same degree that influenza viruses do. A mixture of 50 inactivated rhinovirus types should be able to stimulate neutralizing antibodies against all of them to some degree.<ref>{{cite web |url=https://grantome.com/grant/NIH/R43-AI131750-01 |title=Development of polyvalent inactivated rhinovirus vaccine |year=2017|last1=Tang |first1=Roderick |last2=Moore |first2=Martin }}</ref>