In 1972, long before smallpox was eradicated worldwide, vaccination for the
disease was halted in the United States, where the disease had not been seen
for years. As smallpox was isolated to smaller and smaller regions on the
planet, vaccination was halted in the disease-free parts of the world until
finally mass smallpox vaccination was eliminated entirely, and vaccination
of contacts and in concentric area rings was used to control the few
remaining outbreaks until the disease was finally declared to be eliminated
completely.
It has been proposed here and elsewhere, that perhaps this model suggests
that it would be reasonable to cease vaccination for polio, now that that
disease, too, is on the eve of its eradication. After all, the Americas,
Europe, China and East Asia, and the South Pacific have all been certified
free of wild polio. The disease has been isolated to just seven countries,
with more than 90% of the cases in just Nigeria, Afghanistan, Pakistan and
parts of India. Isn’t it time the rest of the world can cease the program of
vaccination, which, after all, carries known health risks?
The answer is NO.
Smallpox and polio are very different diseases, and the vaccines are
different as well. Smallpox virus is transmitted via the airborne route, and
does not survive long in the environment. This means that the disease can
only be transmitted directly from person to person. Polio is transmitted by
the oral-fecal route, and can survive for weeks or more in contaminated
waste streams. Smallpox causes obvious symptoms in its victims, even in its
mildest forms, so that it is relatively easy to identify an index case and
trace contacts. Polio is so mild as to go undetected in as many as 95% of
infections, so that an infectious traveler could spread the disease over a
wide area, unknown to health authorities. Smallpox vaccine is the live virus
of a related disease, vaccinia, so the public is not exposed to any actual
smallpox virus in the vaccination program. Oral Polio Vaccine (OPV) consists
of mutated live viruses of the three strains of polio. These can
occasionally mutate back into the pathogenic forms of the virus and cause
paralytic polio in the vaccinated persons and in persons exposed to viruses
shed from their intestinal tracts. Smallpox vaccine confers immunity
quickly, and can offer protection even after one is exposed to the disease
virus. Polio vaccination takes longer to be effective and cannot overpower
the pathogenic virus after exposure. Immune suppressed persons, such as HIV
patients and organ donor recipients may be able to carry polio viruses in
their intestines for extended periods of time. One of these “carriers” could
spread polio far and wide in an unvaccinated population. It has been
estimated that as many as 7000 cases of paralytic polio would occur in an
unvaccinated city from one infected person before a vaccination program
could catch up and halt the spread.
Smallpox virus, at the time of the eradication of the wild disease, was
believed to exist only in two or three level-four containment research labs
in the world. (The virus has probably gotten into the hands of terrorist
organizations since then.) There was hope that even the research stocks
could be eliminated at that time. In contrast, polio virus is common in labs
all over the world, and no attempt has been made to document and track where
stocks of it exist. Since a reservoir of the virus is necessary for the
production of vaccine, it will never be practical to eliminate it entirely.
SARS disease information you’ve heard NO WHERE yet but here:
1. HTLV (Human T-cell Leukemia Virus) infection will likely interfere
with established SARS partial immunity and likely allow for the
reactivation of SARS disease in healthy carriers.
2. SARS coronavirus may be passaged from mother to child either in
utero or during neonatal life.
3. Children infected by their mothers with SARS coronavirus will
probably not usually develop SARS but become immune carriers of the
virus for a period of 5-6 months.
4. Recovery from the SARS coronavirus carrier state is likely
associated with a loss of premunition immunity.
5. SARS coronavirus likely targets CD13 (aminopeptidase N) on
cell-surfaces and will cause increase in interferon-alpha,
interleukin-6, soluable CD23, and tumor necrosis factor-alpha. CD64-
people may be more seriously affected. CD14 and CD16 may also be of
interest relative to SARS disease processes.
6. SARS coronavirus may target glial (nerve) cells and sequelae of the
disease may include multiple sclerosis and schizophrenia as the SARS
coronavirus may activate HERV-W retrotransposons in some individuals.
Additionally, there is a likelihood that SARS may later increase
likelihood for development of lymphocytic leukemia in some persons.
7. SARS disease infectivity appears, though caused by a coronavirus,
to be somewhat related to Newcastle Disease Virus, a paramyxovirus of
birds and to Avian infectious bronchitis virus, a coronavirus of
birds. Study of transmission vectors of NDV and AIBV may offer insight
into SARS disease transmission in humans.
8. Individuals may carry SARS coronavirus in their system for as long
as 6 months after recovery; they can be infective to others during
this time.
9. Some individuals are silent carriers of the SARS coronavirus. Class
II Major Histocompatibility Complex Human Leukocyte Antigen genetics
appear to determine who is a carrier and who gets the disease and how
serious the disease symptoms are. Some people may be entirely and
completely resistant to infection by the SARS virus, i.e., likely to
be approximately 1% to 10% of Northern European populations.
10. SARS coronavirus mortality rate may exceed 18% in HLA-DR, -DP, -DQ
predominate countries.
11. Immunosuppressed individuals will not likely get the serious
hyperimmune illness of SARS but they may develop a persistent
infection with SARS coronavirus and be infective to others. This has
implications for HIV+ individuals and disease control/quarantine
policies.