Rapid Responses to:

EDITORIALS: John T Macfarlane and Wei Shen Lim Bird flu and pandemic flu BMJ 2005; 331: 975-976 [Full text]

Rapid Responses: Submit a response to this article

Rapid Responses published:

Global Bird flue threat. What broader prospects to consider?

Dr Wayengera Misaki, Prof Olobo J, Dr kajjumbula H, Dr Kaddu M   (1 November 2005)

Asymptomatic spread of influenza is not proven

Ronald Eccles   (1 November 2005)

Global Bird flue threat. What broader prospects to consider? 1 November 2005
Dr Wayengera Misaki, Study Coordinator MU-UMDNJ Research colloboration., Prof Olobo J, Dr kajjumbula H, Dr Kaddu M Send response to journal: Re: Global Bird flue threat. What broader prospects to consider?	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.
Asymptomatic spread of influenza is not proven 1 November 2005
Ronald Eccles, Professor and Director Common Cold Centre, Cardiff University, Cardiff CF10 3US Send response to journal: Re: 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