The contractile effect of the outer hair cells, activated by the efferent nervous system has been proven to provide a protective effect against acoustic trauma. However, a 2006 study revealed a different protective mechanism for stress conditioning. The study revealed that the stressor (sound, heat, or stress) conditioning increases the receptibility to glucocorticoid, a kind of anti-inflammatory hormone. The effects of glucocorticoid thus mitigate the inflammation from an acoustic trauma that can lead to hearing loss. In fact, high doses of corticoids are often prescribed by physicians after an acoustic-trauma in order to mitigate the inflammatory response. Summarized, sound (or other stressor) conditioning is a pre-emptive medication against cochlea inflammation. It does not make the ear more resistant to noise. It reduces the inflammation caused by the acoustic trauma, which would cause subsequent damages to hair cells. While an anti-inflammatory medication would increase the quantity of anti-inflammatory hormone in the whole body, noise conditioning increases the number of receptors for the anti-inflammatory hormone, and only in the areas where it is much needed (i.e. cochlea). Physiological response

stressor (noise, heat shock or stress) conditioning activates hormonal glands: the HPA axis. Note that the HPA axis is associated to the immune system
this HPA axis activation results in the up regulation of glucocorticoid receptors (GR) in the cochlea and the paraventricular nucleus (PVN) of the hypothalamus. Note that the glucocorticoid hormone is a kind of immune-reaction-inhibitor, including the inflammation reaction.
Enfuvirtide binds to gp41 preventing the creation of an entry pore for the capsid of the virus, keeping it out of the cell.Enfuvirtide is also an activator of the chemotactic factor receptor, formyl peptide receptor 1, and thereby activates phagocytes and presumably other cells bearing this receptor (see formyl peptide receptors). The physiological significance of this activation is unknown. Microbiology
Enfuvirtide is considered to be active against HIV-1 only. Low activity against HIV-2 isolates has been demonstrated in vitro.Variable susceptibility to enfuvirtide has been observed in clinical isolates, with acquired resistance the result of a mutated 10 amino acid motif in viral gp41. Primary resistance, however, has yet to be observed. Clinical use
Indications
Enfuvirtide is indicated for the treatment of HIV-1 infection, in combination therapy with other antiretrovirals, in patients where all other treatments have failed. Dosage forms
By virtue of its peptide nature, enfuvirtide is marketed in injectable form. The lyophilised enfuvirtide powder must be reconstituted by the patient and administered twice daily by subcutaneous injection. Due to the chronic nature of this kind of therapy, this dosage form may be a major problem for the patients adherence to this drug regimen. Adverse effects
Common adverse drug reactions (≥1% of patients) associated with enfuvirtide therapy include: injection site reactions (pain, hardening of skin, erythema, nodules, cysts, itch; experienced by nearly all patients, particularly in the first week), peripheral neuropathy, insomnia, depression, cough, dyspnoea, anorexia, arthralgia, infections (including bacterial pneumonia) and/or eosinophilia.