Bird flu and pandemic flu
BMJ 2005; 331 doi: https://doi.org/10.1136/bmj.38649.389005.DE (Published 27 October 2005) Cite this as: BMJ 2005;331:975
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The Emergency of new viral strains capable of infecting & causing
disease is not a new concept as its dynamics have been widely studied.Its
a known fact today that many emerging viruses have in part or whole existed
in previous reservoirs, and what may really be new to consider are the
broader implications of the imminent global pandemic that may result from
successful & sustainable crossovers. Luckily to date, most of the
crossovers have involved strains of very virulent & thus quickly
"resolving viral infections in the community"--of course by acutely
claiming their victims, but that may not be the case for ever-considering
that mutations (drifts & shifts) and reassortments constantly generate
new viral strains with unknown capabilities.
We have embarked on a journey into the unkown to analyse the
seroprevalence of filoviridae viruses in ugandan NHPs for Ebola &
marburg using RT-based PCR and specific strain genomic analysis.
We think that vaccination at the NHP may help prevent further
outbreaks, besides knowledge of this seroprevalence providing basis for
convincing communities to stay away from NHP niches.
Our Study is based on the following Hypothesis.Funding is still
minimal, and collaborations with the WHO/CDC/et al may be greatly welcome.
Emerging and re-emerging viral infections have been in existence
even before they were isolated or shown to cause disease in humans. They
existed in previous hosts called “natural and reservoir” hosts on which
they depended for the virus-host cell interaction necessary for viral
replication - since all viruses are obligate replicative microbes.
With
an increasing change in variables among the previous hosts and environment
(stability of the virus and chance of contact with new host) there is
adaptation of these viruses (not necessary) through mutations,
recombination and re-assortment to yield new strains able to use new host
(human) cells for replication.
The most susceptible new hosts are those
whose cellular biochemical environments and genetics favor viral
establishment by coding for and producing the energy, metabolites and at
most, in some cases all the enzymes required for replication of the
adapted new strain of virus. Depending on the endogenous tissue
specificity exhibited by a virus however, viral crossovers can
successfully occur between host species of variable biochemical and
genetic homology
Various mechanisms of interaction between previous and
new (human) hosts are required to effect the viral crossover. These may be
direct (as occurs via contact, consumption of meat for ebola VHF or
inhalation of respiratory droplets for Avian flue/SARS) OR Indirect (as
occurs through vectors like arthropods for arboviruses and amplifier -
link hosts like pigs/birds & civet rats for Avian flue /influenza
& SARS).
Of particular Global health importance are not so much these
postulations however, but rather their implications (I0Ps).
I0P.1. All
emerging viruses are zoonotic, with a natural reservoir a more likely
source of the new virus strain than just spontaneous evolution of a new
viral entity. This implies that there are todate various viruses out there
in veterinary reservoirs which have not been isolated or shown to cause
disease in man, but are potential zoonoses to man. Wild ecologic
populations are thus an unexplored source of information regarding viral
infectious diseases and criteria to link human and veterinary programmes
of health is necessary. Experience with veterinary retroviral and other
viral vaccines may be applicable in human situations to control, prevent -
let alone develop human vaccines
I0P.2. The control of viral zoonoses
requires knowledge of the various variables and how they interplay to
increase incidence of zoonotic viral emergence and re-emergence. There is
thus need to strengthen epidemiologic surveillance and concentrate public
health activities in epicenters of new emergent viral infections to study
these variables - South East Asia fro Avian flue/SARS and Gabon & DRC
for ebola VHF.
IOP.3. Innate viral specificity for a particular
cell/tissue type remaining a constant, wherever successful viral
crossovers have been noticed between different species, these crossovers
can play a role in the in the study of evolutionary trends. Thus
restriction of contact between man and his close phylogenetic relatives
like NHPs known to be sources of viral zoonoses can play a major role in
control of emergent viral infections . All activities centered around
possible reservoirs to human zoonotic viruses should be quarantined &
routinely surveyed. IOP.4. Minimizing interactions that increase risk of
zoonotic viral crossovers between identified previous hosts and man can
greatly reduce incidence of emergent viral infections. Restricting human
contact/consumption (of) with caucus of previous hosts for ebola VHF
(NHPs),infected bird for Avian flue & civet rats for SARS can play the
trick. Respiratory droplet inhalation in the later cases may be prevented
by wearing masks as well for Lab scientisits. Arboviruses on the other
hand, which have sometime now not paused any much danger to global Health
over the recents years may be prevented by vector control-spraying with
insecticides and use of Insecticide Treated Nets(ITNs).
Xenotransplantation with amplifier-link host tissue(porcine) should
carefully be watched histo-immunologically, if not avoided to prevent
xenosis.
References:
1.Wayengera Misaki. Emergence of zoonotic viral infections in this
era.why? Abstract book and programme of the international students
conference on emergencies(ISCE) 11-14th Dec,2001:7
2.Wayengera Misaki. The evolutionary adaptation Hypothesis to explain
the origin of ebola VHF. Makerere Medical Journal(MMJ)2002;36:36-37
Competing interests:
The author is part of a team of four scientists aiming to asses the filoviridae serostate of ugandan NHP for Ebola/Marburg viruses & prospects for primary vaccination at the NHP level as a cross-species prevention measure.
Competing interests: No competing interests
Asymptomatic spread of influenza is not proven
Dear Editor,
I note in your recent Editorial on Bird flu and pandemic flu you
state "unlike
SARS flu is highly infectious before patients develop definite symptoms".
I
would like to challenge you on this statement and ask for some hard
evidence
for asymptomatic transmission of influenza. I am aware of the paper by
Fraser et al. (2004) that puts forward a model for the spread of influenza
but
this paper only provides a mathematical model for transmission and does
not
provide any convincing references to support asymptomatic spread of
influenza. There is some older work by RB Couch in the 1970's that states
that viral shedding may sometimes occur before significant symptoms but
one cannot equate viral shedding detected by nasal swabs to transmission
of
infection. My own view is that in order for influenza to transmit from one
person to another there must be exchange of infected airway mucus.
Rhinorreah, coughing and sneezing are important factors in facilitating
aerosol and fomites transmission of infection and I am very doubtful that
any
significant exchange of airway mucus can occur from asymptomatic cases of
influenza. I have recently searched the literature to try and find some
properly
documented cases of asymptomatic spread of influenza and I would be
grateful if you or your readers could provide some hard evidence for this
form of transmission, because as you rightly state in your editorial this
is a
very important issue for infection control of pandemic influenza. I would
have
thought that with influenza being a seasonal problem every year it should
be
relatively easy to follow up a trail of asymptomatic spread of influenza
but I
have not found any convincing clinical evidence for this in the
literature.
Fraser C, Riley S, Anderson RM, Ferguson NM. Factors that make an
infectious
disease outbreak controllable. Proc Natl Acad Sci U S A 2004;101(16):
6146-51.
Competing interests:
None declared
Competing interests: No competing interests