Dengue in French Polynesia

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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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Dengue in French Polynesia: Major Features, Surveillance, Molecular Epidemiology and Current Situation

Dengue Bulletin Vol 22, 1998 75

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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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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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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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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Figure 4. Yearly distribution of dengue in French Polynesia,

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0

100 0

2 0 0 0

3 0 0 0

4 0 0 0

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6 0 0 0

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8 0 0 0

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0 %

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5 0 %

6 0 %

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Numberofcase

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Dengue in French Polynesia

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