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The antibody titers produced were wildly beyond that from natural infection without any explanation as to why. A reasonable explanation is that the manufacturers either knew or suspected that (1) the protection would rapidly wane and thus gamed the test so as to pass the deliberately-short timeframe required to sell them and (2) viral evasion due to mutation was likely.

And one more factor: the IgG antibodies one develops from the injection are not very effective at upper respiratory infections, where you want IgA antibodies present at the infection site.

From Fields Virology (2013), Chapter 14 (Abs = antibodies) :

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Abs present in the systemic circulation efficiently protect internal organs against viruses that are introduced directly into the bloodstream (e.g., HBV and HIV) or that spread via the bloodstream from primary sites of replication such as the respiratory or gastrointestinal mucosa. As mentioned previously, diseases produced by viruses that fall into the latter category (i.e., measles, polio, hepatitis A, rubella, smallpox, and varicella) can be prevented or modified by Ig prophylaxis, often with small amounts of Ab that are difficult to detect in the blood of recipients. Such Abs are relatively easy to induce by parenteral immunization with live or inactivated virus vaccines. In contrast, Abs present in the systemic circulation do not provide efficient protection against viral diseases that are limited to mucosal surfaces unless these Abs are present in high titer. This is because only a small proportion of such Ig molecules traffic from the plasma to the lumenal surface of the mucosal epithelium by transudation. Therefore, to prevent viral diseases that are limited to mucosal tissue, two different strategies can be employed. The first is to induce Abs such as secretory IgA at the mucosal site by virus replication or immunization at that site. The second, and less efficient, strategy is to stimulate a high titer of serum IgG Abs that can protect mucosal surfaces following transudation.

When IgG Abs present in the blood are passively transferred to mucosal surfaces by transudation where they can exert antiviral activity, there is a gradient regarding the ability of serum IgG-derived Abs to restrict virus replication on mucosal surfaces. This gradient is less in lung than it is in the nasopharynx.
IgG Abs, if present in the serum in high enough titer, can provide almost complete resistance to pulmonary replication of RSV; however, resistance in the upper respiratory tract is more difficult to achieve.

Although passively transferred IgG Abs can provide mucosal immunity in the lower respiratory tract, the major mediators of resistance to virus infection of the upper respiratory tract, the larger airways of the lungs, and the gastrointestinal tract are mucosal Abs, many of which are IgAs selectively transported across mucosal surfaces to exert antiviral effects on the lumenal
surface.