It doesn’t matter whether you think viruses are alive or not, the mechanisms that inactivate them are the same that apply to inactivation of many biomolecules in general. In a nutshell, many viruses "die" in air because it is not their physiological environment. HIV spreads via transfer of body fluids, so it hasn’t even had a real reason to evolve towards a form that survives outside the human body (unlike, say, adenoviruses, which often spread via airbourne particles).

I think there are several underlying mechanisms that cause the inactivation of the virus (in air). For example, UV light causes biochemical changes in the microbe’s nucleic acids, such as pyrimidine dimers that render the given nucleotide inactive. Also, mere drying is one mechanism – apparently when drying, the viral proteins get cross-linked or otherwise lose their conformation and the lipid membrane degrades. Since HIV requires its envelope in order to be infectous, this also destroys the infective virus. Finally, RNA (HIV’s genetic material) as such is an unstable molecule (when compared to e.g. DNA), which readily degrades outside its physiological environment. There are quite possibly some other reasons as well, I’ll add them here if I happen to figure them out.

But all in all, HIV virions seem to be particularly fragile and many of them get degraded right after they’ve been assembled or after budding – being exposed to air greatly accelerates the rate of virion destruction.

Please – this was a reasonable question and it deserves more than BS as an answer. Bottom line is that there simply isn’t alot of data on the mechanism of inactivation. Just that HIV preps do lose infectivity.

Evolution doesn’t proceed with a "reason" in mind.

I’ve not seen UV as a mechansim for microbiological inactivation expect for its purposeful application – it’s doubtful that it is central to HIV inactivation upon drying.
And please (!l) don’t offer half baked answers. One would not have thymidine dimers with HIV – it’s an RNA virus – RNA has NO thymidine.
Drying doesn’t provoke "cross linking" of proteins. If anything, drying denatures the tertiary perhaps secondary structure of proteins. Lipid "degrading"? Pretty general – typically one would expect li[pids to oxidize

to add:

An extensive study on the survival of HIV after drying was reported by Resnik and coworkers (Stability and inactivation of HTLV-III/LAV under clinical and laboratory environments. Journal of the American Medical Association 1986;255:1887-91). The purpose of the study was to determine the inactivation rate of HIV under experimental conditions – an objective that required the use of extremely high levels of HIV. The concentrations studied were at least 100,000 times greater than those typically found in the blood of HIV-infected persons. It is not surprising that when such high concentrations of HIV were used, the virus could be detected 1 to 3 days after drying. Upon close examination of these data and from other results that have been obtained by CDC, however, it is clear that drying causes a rapid (within 1 or 2 hours) reduction in virus concentration and renders 90 to 99 percent of the virus inactive.

HIV is very fragile and does not survive well outside the human body. HIV is inactivated by heat and dies after 30 minutes at 56EC (132.8EF). It is also highly susceptible to physical and chemical agents.

If properly stored, HIV is very stable at low temperatures. It can last 7-10 days at 4EC (39.2EF) and months to years at -70EC (-94EF). The Centers for Disease Control and Prevention (CDC) stores purified virus preparations in liquid nitrogen (-200EC or -328EF). In all cases, the stability of HIV depends on the presence of the proper concentration

I’m sorry, what is the BS part of my answer? I meant that it doesn’t matter whether someone thinks viruses are alive or not, because the mechanisms of inactivation remain the same.

UV irradiation for sure inactivates several kinds of microbes, mere sunlight is more than enough for many cases. If you haven’t heard of it, it’s hardly my fault. And can you tell me in which part of my post I said there would be thymidine dimers in HIV? Cytosine is a pyrimidine as well, and it can undergo dimerization as well as deamination under UV irradiation. I said UV light can cause "biochemical changes in the microbe’s nucleic acids", not that it causes "thymidine dimers with HIV". Neither did I say that UV light is the central mechanism of inactivation upon drying. It’s an independent mechanism, it does not matter whether drying is involved or not. Get a grip.

With evolutionary "reason" I simply meant that there has been no pressure towards HIV evolving to an airborne microbe, even you must’ve understood that.

The lipids part: I wrote lipid membrane degrades because it does so. If you want to add something in deeper detail, please do so.

Aaand what comes to protein-cross linking: I stated that proteins get cross-linked OR otherwise lose their conformation – I said this because I wasn’t entirely sure about the mechanism involved here and didn’t have much time to start searching for references. I didn’t state it as a fact that drying cross-links HIV proteins, I stated that this or some other process makes proteins lose their active shape.

So, thanks for you well-baked response to my post. Keep it coming. Only next time maybe actually read the post you’re commenting on and then think if your wannabe witty answers contribute anything useful to the conversation.

to add:

You can also stuff that bottom line of yours to some place where the sun doesn’t shine, because I could find several hundred peer-reviewed articles concerning the mechanisms of inactivation of HIV after a few minutes’ search…

Typical – offers nothing and tells others to stuff it. Considering your ignorance of RNA chemistry, I think this pretty much confirms your level of expertise.

The question was inactivation upon exposure to air – effectively drying. If you have information share it. If not – and as you said – stuff it.

Wondering what molecule could be attached to a methyl group to cap (inactivate) any of the 8 main HIV genes, thereby not allowing them to produce gene product thus rendering the virus benign and furthermore allowing vaccination with doses of benign forms of the HIV virions allowing the body to create antibodies to the actual virus. This would allow cell initiated immunity to occur immediately upon recognition and identification of virus particles inside the human body. Don’t understand fully why it is that some molecule cannot be developed with a high affinity to the GP160 (GP120 + GP41) complex that would effectively avoid other receptors on other cells?