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74 Dengue Bulletin Vol 22, 1998
Dengue in French Polynesia: Major Features,
Surveillance, Molecular Epidemiology and
Current Situation
By
Eliane Chungue, Xavier Deparis & Bernadette Murgue
Institut Territorial de Recherches Mdicales Louis Malard
P.O. Box 30, Papeete, Tahiti, French Polynesia,
Fax : 689-43 15 90, e-mail: [email protected]
Abstract
The emergence of dengue epidemics worldwide has paralleled the expansion of the mosquito
vector Aedes aegypti,along with jet air travel and increased urbanization. All the four dengue
virus serotypes (DEN-1, 2, 3 and 4) have occurred in epidemic form during the past 50 years in
French Polynesia. The first epidemic with a known serotype was due to DEN-1 which occurred in
1944 during World War II. The disease disappeared from the Eastern Pacific after a Pacific-wide
pandemic, but a series of epidemics occurred at short intervals during two decades: DEN-3 in
1964-1965, DEN-2 in 1971, DEN-1 in 1975-1976, and DEN-4 in 1979. From 1980 to 1988, the
transmission of DEN-4 continued at a very low level until the resurgence of DEN-1 and DEN-3 in
back-to-back epidemics in 1989. In 1996, DEN-2 reappeared in Tahiti and spread further into
New Caledonia, the Cook Islands, Tonga, Samoa and Fiji.
As in most Pacific countries, epidemics with only one serotype have occurred in French
Polynesia. Each time, the genetic analysis of the causative viruses showed that the current epidemic
_________________________
Reproduced from Pacific Health Dialogue 1998, 5(1):154-162 with the permission of the Editor
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was due to the introduction of a genotype which was different from the viruses recovered from the
past epidemics. These observations emphasize the need for an active system of clinical and
virological surveillance for the prevention and control of epidemics, together with molecular
characterization of the viruses as part of the investigation of a dengue epidemic. As of now, a new
genotype of DEN-2, different from the one involved in the 1970s, is disseminating throughout the
Pacific region.
Keywords: DF/DHF, DEN-1,2,3,4, epidemic, molecular epidemiology, French Polynesia.
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Introduction
French Polynesia, situated in the South
Pacific Ocean, consists of five
archipelagos (Society, Tuamotu,
Gambier, Austral and Marquesas
islands) comprising 120 islands, of
which only 66 are inhabited. Most of
the population is concentrated in the
Society archipelago which
encompasses the Windward and the
Leeward islands. Tahiti, the largest
island of French Polynesia in the
Windward group, contains the Capital,
Papeete. During the past 40 years the
population of French Polynesia has
undergone a dramatic increase. Since
1946, it has trebled in 30 years, and it
has doubled between 1966 and 1988.
The last census (1996) recorded a
population total of 219 521 which is
unequally distributed: 74% of it is
concentrated in the Windward Islands,
especially on Tahiti, of which 77% live
in the urbanized Papeete. In all areas
the climate is hot and tropical. A hotrainy season from November to April
alternates with a cooler, drier season
from May to October. The annual
average temperature and rainfall in
Tahiti is 25.7C and 2 m, respectively.
These climatic conditions are
consistent with the year-round
mosquito breeding.
Epidemiological features
Epidemic pattern
Dengue fever has been known
clinically in French Polynesia since the
nineteenth century, with documented
epidemics in 1852, 1870, 1885 and
1902(1,2,3). The first outbreak of
dengue in Tahiti of a known serotype
occurred in 1944 as part of the
Pacific-wide spread of the disease
caused by DEN-1 during World War
II(4). The disease disappeared from the
Eastern Pacific after the pandemic and,
as far as is known, did not reappear
until 1964 and 1969, when DEN-3
was involved(5,6). From that time on,
epidemics have occurred at shorter
intervals: DEN-2 in 1971, DEN-1 in
1975 and DEN-4 in 1979 were
successively epidemic(7,8,9). With the
exception of the DEN-2 outbreak,during which severe haemorrhagic
cases and three deaths were observed
on Tahiti in 1971, mildness of the
disease characterized these past
epidemics. A recent succession of
epidemics took place after nine years
of continued transmission of DEN-4.
Back-to-back epidemics involving
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DEN-1 and DEN-3 occurred in 1988-
1989. It is noteworthy that dengue
haemorrhagic fever/dengue shock
syndrome (DHF/DSS) occurred in the
latter epidemic (11 fatalities) whilemildness characterized the former.
These viruses were spread throughout
the Pacific region with varying degrees
of disease severity(10).
Epidemics with only one serotype
have occurred. Each epidemic
serotype replaced the previous
serotype that had been transmitted
during the inter-epidemic period.
Simultaneous transmission of bothserotypes was only observed for a
short period of time (2-4 months)
when the epidemic serotype was
taking place. During these periods,
co-circulations were demonstrated for
DEN-2/DEN-1 in 1975, DEN-1/DEN-4
in 1979, DEN-1/DEN-3 in 1989, and
DEN-3/DEN-2 in 1996. The endemic
virus was generally swept out 7 weeks
to 4 months after the recognition ofthe new epidemic. This is illustrated
by Fig.1a and Fig.1b.
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0
5 0
100
150
2 0 0
2 5 0
3 0 0
3 5 0
D J F M A M J J A S O N D J F M A M J J A
Numberofisolate
Dengue 1
Dengue 3
1988 1989 1990I I
Figure 1a. DEN-1 and DEN-3 epidemics (1988-1990):
Monthl distribution of den ue virus serot es
0
50
100
150
200
250
300
350
J F M A M J J A S O N D J F M A M J J A S O
Dengue 3
Dengue 2
1996 1997
Numbero
fisolate
I
Figure 1b. DEN-2 epidemic (1996-1997):
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Morbidity and mortality
Although accurate data regarding
morbidity are not available, a review
of published and unpublished
literature allowed us to obtain
estimates of dengue infection in the
Windward Islands during the major
epidemics which occurred between
1944 and 1997 (Table 1). Estimated
morbidity rates were calculated by
using the data obtained by serological
and/or epidemiological surveys. The
estimation of the attack rates involved
antibody prevalence in cohorts of
susceptible populations and
measurements of absenteeism in
schools and government and business
offices. The serological attack rate was
generally around 50% as determined
immediately after the epidemic
transmission. According to clinical and
serological surveys, the proportion of
asymptomatic infections was
estimated to be 30%(8,11,12). During an
outbreak the mortality rate is usually
low (see Table 1). The morbidity trendof the epidemics is also illustrated by
the number of (i) clinical cases
reported by physicians (reported
cases), (ii) cases for which a request
for laboratory confirmation is made
(suspected cases), and (iii) virologically
and/or serologically confirmed cases
(Table 2). The annual incidence rate
during the inter-epidemic periods
(endemic transmission) is unknown.
One study that concerned the long
inter-epidemic period between 1980
and 1987 showed an acquisition rate
of dengue antibodies of 3% per year in
a cohort of susceptible children(13).
Table 1. Morbidity and mortality of dengue during major epidemics between
1944 and 1997 in the Windward Islands (French Polynesia)
Year of
epidemic
Serotype
Population
Windward Is.
1000s)
Estimated
morbidity
rate( )
No. of fatal
cases
No.of
infected
persons
1000s)
1944 DEN-1 29.8 62 - 26
1964-65 DEN-3 55.2 20 - ND*
1969 DEN-3 79.1 ND* - ND*
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1971 DEN-2 84.5 50 3 42.2
1975-76 DEN-1 94.6 25 - 34.1
1979 DEN-4 104.2 25 - 37.5
1988-89 DEN-1 140.3 17 - 35.1
1989-90 DEN-3 143.9 25 11 49.5
1996-97 DEN-2 162.6 19 1 43.5
*ND: not determined.
Table 2. Dengue cases reported during the epidemics in French Polynesia, 1964-1997
Number of
Year of epidemic Serotype
Reported cases* Suspected cases Confirmed cases
1964-65 DEN-3 1358
1969 DEN-3 72
1971 DEN-2 12943
1975-76 DEN-1 2032 2018 694
1979 DEN-4 7489 1783 630
1988-89 DEN-1 6034 4836 1976
1989-90 DEN-3 6330 5583 1357
1996-97 DEN-2 7230 4424 2027
data not available; *Institut Malarde & Direction de la Sante
Transportation and spread
of virus
In addition to the lack of effective
mosquito control, the origin of the
Pacific-wide pandemic of DEN-1
(1941-1945) was very likely related to
intensive movements of human
populations among and into areas that
were permissive to dengue
transmission during World War II.
Hence, in 1944, an extensive epidemic
of dengue occurred in the Society
archipelago, French Polynesia.
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Together with entomological surveys
in other Pacific islands(14,15,16), the
evidence of experimental transmission
of dengue virus between monkeys
suggested that Aedes polynesiensisserved as a natural vector in the past
epidemics in French Polynesia(14).
Conversely, the geographical
distribution of the disease and the
entomological surveys carried out
during the post-war epidemics (1964-
1996) were more consistent with the
role of Ae. aegypti as a vector. For
instance, while Ae. aegypti was
reported in 1953 in Tahiti, itspresence had expanded progressively
throughout French Polynesia, which
was coincidental with the advent of
inter-island air connections: in the
1970s in the Tuamotu, in 1982-1986
in the Marquesas Islands, and in
1979-1986 in the Austral Islands(17).
The size and frequency of dengue
epidemics are related directly to social
and economic development, especially
urbanization(18,19). For instance, the
first urbanized locale, Papeete,
became so in 1850 during the
European colonization. Coincidentally,
the first occurrence of dengue on
Tahiti was reported in 1852. The
disease was limited to Papeete which
had been recently urbanized with an
increased seaport activity. In the
1960s, important changes in the
ecology of dengue in French Polynesia
occurred after the construction of the
international airport in 1960-1961.This event suddenly brought French
Polynesia into the modern era, with
accelerated urbanization that
paralleled an increasing number of
dengue outbreaks. The increase of
population in Papeete and its
surrounding localities comprised of
workers recruited from the rural part
of Tahiti and from neighbouring
islands. Between 1956 and 1988 thepopulation of Tahiti rose from 50% to
76% of the total population of French
Polynesia; of these, 79% resided in
urban areas. The expansion of Papeete
led to the growth of adjacent suburbs.
At this time, the metropolitan Papeete
lied along a 40 km coastal border only
a half kilometre wide.
The first re-introduction of
dengue viruses was related to multiple
factors: increased jet air travel, high
density of susceptible population in
urban areas, and lack of mosquito
control. Papeete was hit by a DEN-3
epidemic in 1964, as was Makatea
island, a nearby island of the Tuamotu
archipelago whose urban areas were
subjected to exploitation of
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phosphates. Regular exchanges
existed between these two sites, in
both of which Ae. aegypti were
abundant. The limited transmission
within these areas was apparentlyrelated to the sparse distribution of
Ae. aegypti in most islands of French
Polynesia(5). A flare-up of DEN-3 was
reported in 1969 in Papeete(6).
The speed and frequency of
human exchanges by jet air travel
make possible the introduction of
dengue viruses by a dengue-infected
traveller from hyperendemic areas. A
parallel has been observed between
the spread of dengue viruses and the
route and frequency of air travel
between the infected and the
permissive areas within the Pacific
region(20). This was exemplified by the
epidemics which occurred in the
Pacific islands in the 1970s, which
always emerged from countries/areas
which had intensive international
traffic. The disease has spread
secondarily from these points to
neighbouring island countries. For
instance, in 1979 the first occurrence
of DEN-4 outside Asia was observed
on Tahiti. Three years later, DEN-4
had spread to many islands of the
Pacific. At the country level, in French
Polynesia, the geographical diffusion
of the epidemics may be seen in the
dynamics of the recent epidemics. Fig.
2 shows clearly that the DEN-1
epidemic in 1988-1989 moved from
the Windward Islands to the LeewardIslands and on to the Marquesas and
Austral Islands(21). Furthermore, DEN-
3 was first detected in the tourist
island of Bora Bora in the Leeward
Islands, and spread subsequently to
Tahiti, then to the remote
archipelagoes (21). These situations
were consistent with the fact that
inter-island air travel was more
intense between Tahiti and theLeeward Islands than with the
Marquesas and Austral Islands.
Clinical features
The disease has been generally mild.
However, dengue illness caused by all
four serotypes is naturally
accompanied by haemorrhagic
manifestations (22). In most epidemics,
a proportion of cases presented with
minor haemorrhagic signs:15% in
1964 (DEN-3), 4% in 1969 (DEN-3), 3%
in 1971 (DEN-2), 15% in 1975-1976
(DEN-1), 5% in 1989 for epidemic
DEN-1, 14% for epidemic DEN-3, and
18% in 1996-1997 for DEN-2. The
two occurrences of severe
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Dengue Bulletin Vol 22, 1998 83
manifestations requiring
hospitalization were in 1971 (33
cases, 3 fatalities) and 1989-1990
(401 cases, 11 fatalities). The 1971
epidemic involved mostly adults (63%)
while children represented 69% of the
cases in 1989-1990, an outbreak in
which haemorrhagic manifestations
were observed among 59% of the
hospitalized children. In 1996, among
the 232 hospitalized children, the
number of severe forms was low (19
cases), and the proportion of children
presenting with haemorrhagic
manifestations was 36%. Only one
death (adult) was reported(5,6,7,8,10,23).
Socioeconomic impacts
In islands with limited populations,
dengue fever is generally an epidemic
disease. In Asia, where the occurrence
of DHF/DSS is frequent, the social and
economic cost is high (US $31.48
million per year in Thailand(24)).
However, epidemics of the classical
disease are not to be overlooked. For
instance, during the last epidemic of
DEN-1 in French Polynesia, of the 161
subjects from whom a reply to the
question about the number of days
absented from work was obtained,
125 indicated a 3-5 days of absence.
0
100
200
300
400
500
51 52 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16
Calendar week 1988-1989
Windward Is.
Leeward Is.
Marquesas and Austral Is.
Numberofreportedcas
Figure 2.DEN-1 epidemic (1988-1989): Geographical distributionof reported cases, by week
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Moreover, in the 1996-97 DEN-2
epidemic, the direct costs were
estimated to be US $2.5 million,
including laboratory costs,
hospitalization, and medical care. Theindirect costs, including morbidity-
related absenteeism from work, the
cost of lost production and prevention
and control activities was around US
$1.98 million. The estimated total cost
worked around US $4.48 million (i.e.
US $20 per inhabitant). From this
study, it was evident that the
estimated total cost of the 1989-90
DEN-3 epidemic, including theDHF/DSS cases, was US $40 per
inhabitant, whereas the estimated cost
of the 1988-89 DEN-1 epidemic was
US $15 per inhabitant. Estimation of
the costs for loss of tourism was not
made.
Surveillance, prevention
and control
Before 1975, the DHF epidemics did
not benefit from any special control
programme. They were generally
explosive and ended after exhaustion
of the susceptible population. In 1975,
Tahiti was expected to have DEN-1
virus reintroduced from Fiji. With the
efforts of both regional (South Pacific
Commission) and local authorities, a
network of dengue control and
surveillance was set up. Subsequent
funding supported the development of
a community-based vector controlprogramme. Despite the implementa-
tion of preventive measures, an
epidemic occurred a short time later.
Epidemic control involved adulticiding
of mosquitoes using ultra low volume
(ULV) spraying of insecticides.
Larvicidal source reduction measures
involved the destruction or treatment
by insecticides of breeding sites.
Educational programmes accompaniedthese measures(8). During the 1979
DEN-4 epidemic, similar measures
were implemented. After these series
of epidemics, the control programme
was maintained at a minimum level
which comprised continued health
education and limited entomological
surveillance at the international airport
and at a few sentinel stations.
Finally, the only constant and
immediately available surveillance
system is the laboratory-based
system. Laboratory capabilities were
reinforced, and modern and rapid viral
and serological analyses were made
available. Urgent diagnosis of
suspected DHF/DSS was carried out by
reverse transcriptase polymerase
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chain reaction (RT-PCR), allowing a
result within as little as one day(25).
Since 1988, the surveillance of dengue
fever has been based on the
monitoring of (i) cases reported byphysicians; (ii) suspected cases; and
(iii) confirmed cases. Trends of
dengue activity and the virus serotype
are continuously monitored.
Actually, the weekly incidence of
suspected cases constitutes a valuable
indicator of dengue activity(26,27). Since
all the diagnoses are made only in our
laboratory, the data are immediately
available. A sudden rise in laboratory
requests precipitates an immediate
telephone survey among sentinel
physicians. In addition, through a small
group of selected sentinel physicians,
any increase in dengue-like illness is
reported and investigated. Blood
specimens are obtained from
representative cases and processed to
detect dengue infection by virus
isolation or RT-PCR and/or dengue IgM
antibody detection. In addition,
information on dengue activity in the
Pacific region is taken into account in
order to stimulate awareness in the
medical community or to set up timely
sentinel surveillance, as happened in
1996 when DEN-4 was detected in New
Caledonia(28). Subsequently, DEN-2 was
detected instead.
The detection of a serotype
different from the one which is
endemically transmitted constitutes a
very important feature while
considering whether further epidemic
transmission might occur. A
retrospective analysis of the situation
in French Polynesia in recent years
shows that a new epidemic followed
each detection of a new serotype in a
sizeable susceptible population in a
country where mosquitoes were always
present. In 1988, the first isolation of
DEN-1 in Tahiti island intervened
during a nine-year inter-epidemic
period of a low-level incidence of DEN-
4(11). The epidemic peaked a few weeks
after, and the disease spread
throughout most of the islands of
French Polynesia. The first isolation of
DEN-3 was observed in April 1989 in
Bora-Bora island, then in June 1989 in
Tahiti island. The epidemic was
recognized in August in Tahiti(21).
Furthermore, the recent DEN-2
epidemic peaked in January 1997 after
the first case was detected by
laboratory survey in August 1996.
Thus, virological surveillance is of
importance for an early warning
surveillance system.
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Molecular epidemiology
By using molecular techniques, the
transmission pathways of the viruses
have been suggested and seem to
corroborate with the descriptive
epidemiology. Analyse of genome
sequence relatedness demonstrated
genotype groupings among all four
DEN virus serotypes(29). Thus, one to
five genotypes were defined among
virus strains isolated in different
geographic areas and over periods
ranging from 33 to 53 years. Each
genotype seems to have a defined
focus of endemicity. However, certain
genotypes appeared to have been
transported to another part of the
world where they became established.
Different transmission pathways of
these viruses around the world are
pointed out, and co-circulation of two
or more genotypes in the same
geographic region has been observed,
especially for DEN-2 viruses. The first
genetic evidence of the existence of a
sylvatic cycle of dengue virus, clearly
different from outbreak viruses, was
demonstrated, and further confirmed
by molecular analysis(30,31). Owing to
the current circulation of dengue
viruses in our region, the molecular
epidemiology of DEN-2 viruses is
particularly worthy of emphasis.
Nucleotide sequencing of
different parts of the genome as short
fragments or entire genes (prM, E or
NS3) allowed several authors to
perform comparative analysis of a
large variety of dengue virus strains.
Sequence data obtained recently in
our laboratory or those retrieved from
published databases were compared
within each serotype virus. Hence,
fragments of the E protein gene of (i)
180 nucleotides (nt 82 to 261) from
DEN-1 and DEN-4 viruses, (ii) 198
nucleotides (nt 85 to 282) from DEN-2
viruses, and (iii) 195 nucleotides (nt
73 to 267) from DEN-3 viruses were
compared(29). A divergence of 6%
within the studied region was taken as
a cut-off point for virus groupings.
Three genotype groups were
defined for DEN-1 viruses, and
clustering of virus isolates for which
linkages would be expected on
epidemiological grounds was
observed(32). Genetic relationships
were detectable over a 50-year span
(Hawaii, 1944, to the Indian Ocean,
1993). For instance, earlier epidemic
strains from the Pacific (1974-1978)
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clustered in genotype 1 while recent
epidemics strains from French
Polynesia and New Caledonia (1988-
1989) and the Comoro Islands
(1993), as well as from FrenchGuiana, Guadeloupe, Puerto Rico,
Brazil, Peru, Nicaragua and Cuba, fell
in genotype 2 (as do the American
strains). Therefore, it is likely that the
recent epidemics of DEN-1 in the
Pacific region are due to the
introduction of a new variant of virus
rather than the re-emergence of a
strain derived from mutation through
silent transmission. Furthermore, a
high level of dissemination of DEN-1
genotype 2 during recent years, as
shown by the clustering of the virusesrecently isolated in countries that
have ties with French tropical
countries (French Guiana, French
Pacific territories, Comoro Islands)
was suggested, although the
direction of the spread was not
determined.
Figure 3. Molecular epidemiology of DEN-2 viruses
Dengue 2
SOMALIA 84
INDONESIA 76
SRI LANKA 85aSRI LANKA 85bSRI LANKA 90a
SRI LANKA 89SRI LANKA 90b
JAMAICA 83
VIETNAM 87
PHILIPPINES 83
TAIWAN 87
NEW GUINEA 44
THAILAND 64
TAHITI 96
PUERTO RICO 69
INDIA 57
TRINIDAD 57
TONGA 74
BURKINA FASO 83
BURMA 76
FRENCH GUIANA 90
THAILAND 80d
TAHITI 75
SENEGAL 74
SENEGAL 81
BURKINA FASO 80
0 2 4 6 8 10 12 14 16 18 20
% Divergence
CUBA 81
VIETNAM 96
COOK 97NEW CALEDONIA96
TORRES STRAIT 96
QUEENSLAND 92
1
2
3
4
5
Dengue 2
SOMALIA 84
INDONESIA 76
SRI LANKA 85aSRI LANKA 85bSRI LANKA 90a
SRI LANKA 89SRI LANKA 90b
JAMAICA 83
VIETNAM 87
PHILIPPINES 83
TAIWAN 87
NEW GUINEA 44
THAILAND 64
TAHITI 96
PUERTO RICO 69
INDIA 57
TRINIDAD 57
TONGA 74
BURKINA FASO 83
BURMA 76
FRENCH GUIANA 90
THAILAND 80d
TAHITI 75
SENEGAL 74
SENEGAL 81
BURKINA FASO 80
SENEGAL 74
SENEGAL 81
BURKINA FASO 80
0 2 4 6 8 10 12 14 16 18 20
% Divergence
CUBA 81
VIETNAM 96
COOK 97NEW CALEDONIA96
TORRES STRAIT 96
QUEENSLAND 92
1
2
3
4
5
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The maximum divergence over
the E protein gene fragment was
approximately 20% among DEN-2
viruses. The dendrogram shown in
Fig. 3 depicted five genotypic groupsand agreed generally with previously
published phylogenetic trees(30,31,33).
Two genotypes have been
involved in the Caribbean. The
Jamaican genotype (genotype 2) was
confirmed as to be related to virus
strains from South-East Asia (97.5%
similarity with Vietnamese 1974 and
1996 strains). As mentioned byGuzman et al.(33), the Cuban strain
(1981) was closer (98% similarity) to
the old New Guinea C strain (1944)
and clustered in the same genotype 2.
The Puerto Rican strain is shown to be
transmitted in the Caribbean, Central
America, India, and the South Pacific
(Tonga 1974, Tahiti 1975) within the
genotype 4. Interestingly, the recent
virus isolated during the actual
epidemic on Tahiti in 1996 falls into a
new genotype (genotype 3) together
with recent isolates from New
Caledonia. Data sequence from D.
Phillipps (personal communication)
allowed also the classifycation of 1992
Queensland, 1997 Cook Islands and
Samoa isolates in the same genotype.
This new genotype is significantly
distinct from the previous virus
groups (9% divergence with genotype
4). The Tahiti 1996 strain presented a12.5% difference with the earlier
Tahitian virus (1975), and agreed with
the evidence of a virus recently
introduced rather than to the
hypothesis of a new variant derived
from earlier virus. Its closer genotype
is genotype 1, in which isolates from
Torres Strait (D. Phillipps, personal
communication), Burkina Faso or Sri
Lanka fell.
Four genotypes were defined
among 30 isolates of DEN-3 viruses
with the entire gene or restriction
analysis(34). The first group contained
isolates from the South Pacific (1988
to 1995), Singapore (1973) and
Indonesia (1973 to 1991). The second
group comprised the viruses from
Asia (1956 to 1995) including the
reference strain H-87 and the
Vietnamese strains (1974 and 1995).
The third was composed of one isolate
from Thailand (1971). The fourth
genotype included the early strains
from French Polynesia (1964 to 1969)
and from Puerto Rico (1963).
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Maximum divergence over the studied
region was approximately 12% and
corresponded to the distance between
the early (1964 and 1969) and recent
(1989 to 1995) Polynesian/NewCaledonian DEN-3 strains. Hence, it is
unlikely that the recent isolates result
from a genetic mutation of the
remaining endemic virus, since no
DEN-3 virus has been isolated within a
20-year period. Therefore, as for
DEN-1, these data suggest that the
recent epidemics in the Pacific are due
to the introduction of a new variant
virus rather than the re-emergence of
a strain derived from mutation
through silent transmission. Moreover,
there is a sequence similarity between
a New Caledonian strain (1988)
recovered four months before the
recognition of the epidemic. This
favours the hypothesis of the
emergence of DEN-3 epidemics in the
Pacific from Indonesia via NewCaledonia after several months of
latency.
DEN-4 viruses seem to occur as a
single genotype around the world. The
sequence variation in the same region
of the E protein gene among DEN-4
viruses was lower (4.9%) than among
the three other serotypes since the
maximum divergence was 20% for
DEN-2 viruses, 12% for DEN-3 viruses,
and 6.9% for DEN-1 viruses. However,
microheterogeneity was observedwithin DEN-4 geographic strains that
clustered in two subgroups.
Interestingly, the recent isolate from
New Caledonia (1996) appears to be
more closely related to the viruses
from Indonesia. This variant was
present for only a few weeks in early
1996. Whether its failure to be
transmitted intensively is related to a
weak adaptation of the virus to its
vector and /or host or to unfavourable
climatic conditions, combined with an
active vector control programme, is
difficult to state (M. Laille,
unpublished data). Moreover,
transportation of virus from one
continent to another is illustrated by
the isolation of the Haiti 1981 strain in
Senegal from a patient who had justarrived from Haiti(31).
These studies demonstrated that
dengue viruses could be identified and
classified in genotypic groups that
may circulate concurrently in the same
region. Moreover, in some instances,
the origin of the newly introduced
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90 Dengue Bulletin Vol 22, 1998
virus has been suggested. For
instance, close relationships between
the Polynesian strains (1964 and
1969) and the Puerto Rican (1963)
DEN-3 strain or between thePolynesian (1975) and Puerto Rican
(1969) strains or Trinidad (1957) DEN-
2 strains, suggest possible virus
exchanges between the Caribbean and
the South Pacific owing to the frequent
trades from Europe via the Panama
channel. The South Pacific-American
connection was also suggested by the
close genetic relationships between
DEN-4 viruses (99 to 100% homology).In more recent years, the introduction
of a new virus in the South Pacific
seems to be more related to frequent
air travel exchanges with Indonesia
(DEN-3 in 1989, and DEN-4 in 1996).
Each time, a new epidemic was due to
the introduction of a new genotype.
The current DEN-2 virus spreading
from Tahiti to New Caledonia and the
Cook Islands belongs to the same
genotype. This emphasizes the
efficient dissemination of viruses
among these island countries through
intra-regional travel. Furthermore,
certain genotypes of the viruses have
been associated with severe disease
potential. However, it is still unclear
whether any particular molecular
change is involved in the
pathogenicity of DHF/DSS.
Current situation
Fig. 4 illustrates the yearly distribution
of the suspected and confirmed
dengue cases from 1988 to 1997.
Since its recent introduction, DEN-2
has been continuously transmitted. In
view of the risk of epidemic dengue,
when considering the time elapsed
since the last epidemic of a given
serotype and the size of the
population born subsequently, FrenchPolynesia is at high risk for the
reintroduction of DEN-4, and to a
lesser extent, of DEN-1. Retrospective
observations concerning the
epidemiology and control of the
recent epidemics showed that
emergency adulticiding and larvicidal
control have to be applied
immediately after the detection of the
first emergence of either virus.
Advantage may be taken of the usual
one-to- several months of the time
lag before the recognition of an
epidemic.
In conclusion, improved
laboratory-based surveillance, genetic
investigation of circulating viruses,
disease surveillance (specific and
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Dengue Bulletin Vol 22, 1998 91
febrile diseases), health education
programmes, and vector control
programmes must be promoted for the
better prevention and control of
epidemics.
Acknowledgments
The authors thank C. Roche, O.
Cassar, F. Laur, A. Babinet, K. Laille
and JF Schnee for their collaboration,
and D.Q. Ha of Pasteur Institute, Ho
Chi Minh City and M. Laille from
Institut Pasteur de Nouvelle Caldonie
for providing the 1996 virus strains.
The authors also thank N. Maruhi and
D. Pons for their secretarial
assistance.
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