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infection with B virus, the infected individual had contact with rhesus
macaques and in only some of those cases did he or she also have contact
with long-tailed macaques (Smith et al ., 1998 ). Therefore, it is not pos-
sible to clearly indentify whether long-tailed macaques have ever truly been
involved in a human infection of B virus. In the 1990s, concern over B virus
infection led primate laboratories to institute stricter guidelines to protect
lab workers from agents transmissible in primate body fluids (Holmes et al .,
1995 ). They appear to be successful, since no cases of B virus have been
reported since 1996.
Interestingly, no human B virus cases have ever been documented out-
side the laboratory context, in spite of the abundant human-primate contact
that occurs in many countries in south and Southeast Asia (Engel et al .,
2002 ; see also Jones-Engel and Eberle, unpublished data in 2006a ). A pos-
sible explanation for this observation is that only the strain of B virus cir-
culating among laboratory macaques is capable of causing severe human
disease. There are some data that suggest that this hypothesis should be
further explored. Smith and colleagues showed the presence of four distinct
genotypes of B virus in four species of macaques, M. mulatta, fascicularis,
nemestrina and fuscata (Smith et al ., 1998 ). However, Smith and others
have also noted that at least within a laboratory setting there was evidence
of cross-species transmission of B virus between rhesus and long-tailed
macaques (Hilliard and Weigler, 1999 ). The possibility that a pathogenic B
virus resulted from the mixing of a variety of macaque species in laboratory
settings also exists.
The above hypothesis may explain the lack of reported human herpes B
infections in south and southeast Asia, where human/macaque contact is abun-
dant. Alternatively, some have theorized that human infection with B virus
actually does occur, but goes undiagnosed owing to poor disease reporting,
or mild symptomatology, perhaps as a result of high titres of anti-Herpes sim-
plex antibodies in these human populations (Elmore and Eberle, 2008 ; Hilliard
and Weigler, 1999 ; Ohsawa et al ., 2002 ). However, this hypothesis fails to
explain the lack of reported B virus disease among the hundreds of thousands
of visitors to Asia who may be exposed to the virus through bites, scratches,
and mucosal contact with macaque body fluids (Fuentes, 2006 ; Fuentes and
Gamerl, 2005 ). A portion of these visitors return to their home country and
seek medical evaluation/treatment, yet no cases of B virus have been reported
(Gautret et al ., 2007 ; Ritz et al ., 2009 ).
Notwithstanding these scientific considerations, fear of B virus infection
has led to the occasional and, we would argue, irrational culling of macaques.
For example, in March 2000, after testing rhesus macaques at the Woburn
Safari Park in the UK for herpes antibody and learning, not surprisingly,
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