Jpn. J. Infect. Dis., 52, 1999

Laboratory and Edpidemiology Communications

Prevalence of Drug Resistance-Related Mutations among HIV-1s in Japan

Wataru Sugiura*, Masakazu Matsuda, Hanae Abumi, Kaneo Yamada 1, Masashi Taki 2, Masaaki Ishikawa 3,Takuma Miura 4, Katsuyuki Fukutake 5, Kengo Gouchi 6, Atsushi Ajisawa 7, Aikichi Iwamoto 8,Hideji Hanabusa 9, Junichi Mimaya 10, Junki Takamatsu 11, Noboru Takada 12, Eizo Kakishita 13,Akira Yoshioka 14, Seizaburou Kashiwagi 15, Akira Shirahata 16 and Yoshiyuki Nagai

AIDS Research Center, National Institute of Infectious Diseases, 4-7-1, Gakuen, Musashimurayama-shi,
Tokyo,1Institute of Medical Science, St. Marianna University School of Medicine, 2-6-1, Sugao,
Miyamae-ku, Kawasaki-shi, Kanagawa, 2Dept. of Pediatrics, St. Marianna University, 
School of Medicine, 2-6-1, Sugao, Miyamae-ku, Kawasaki-shi, Kanagawa, 3Third Department
of Internal Medicine, Tohoku University, School of Medicine, 1-1, Seiryo-cho, Aoba-ku, Sendai-shi,
Miyagi, 4Department of Pediatrics, Haga Red Cross Hospital, 2461, Dai-machi, Mooka-shi, Tochigi,
5Department of Clinical Pathology, Tokyo Medical University, 6-7-1, Nishishinjuku, Shinjuku-ku,
Tokyo, 6Department of Internal Medicine, Teikyo University, School of Medicine, 2-11-1, Kaga,
Itabashi-ku, Tokyo, 7Department of Infectious Diseases, Tokyo Metropolitan Komagome Hospital, 
3-18-22, Honkomagome, Bunkyo-ku, Tokyo, 8Department of Infectious Diseases, Institute of 
Medical Science, The University of Tokyo, 4-6-1, Shiroganedai, Minato-ku, Tokyo, 9Department 
of Hematology, Ogikubo Hospital, 3-1-24, Imagawa, Suginami-ku, Tokyo, 10Division of Hematology-
Oncology, Children's Hospital of Shizuoka Prefecture, 860, Urushiyama, Shizuoka-shi, Shizuoka,
11Department of Blood Transfusion, Nagoya University Hospital, 65, Tsurumai, Syowa-ku, 
Nagoya-shi, Aichi, 12Division of Blood Transfusion Services, HiroshimaUniversity Medical 
Hospital, 1-2-3, Kasumi, Minami-ku, Hiroshima-shi, Hiroshima, 13 Second Department of Internal
Medicine, Hyogo College of Medicine, 1-1, Mukogawa-cho, Nishinomiya-shi, Hyogo, 
14Department of Pediatrics, Nara Medical College, 840, Shijo-cho, Kashihara-shi, Nara, 
15 Department of General of Medicine, Kyushu University Hospital, 3-1-1, Maidashi, Higashi-ku, Fukuoka,
16 Department of Pediatrics, University of Occupational and Environmental Health, 1-1, Iseigaoka, 
Yahatanishi-ku, Kitakyushu-shi, Fukuoka.

Communicated by Hiroshi Yoshikura

(Accepted February 23, 1999)

   Nucleoside analogue reverse transcriptase inhibitors (NRTI) and protease
inhibitors (PI) began being used in Japan for treatment of HIV-1 infected patients
shortly after they were found to be effective (1). Highly Active Anti-Retroviral
Therapy (HAART) (2) is now recommended. One of the problems in using these 
anti-HIV-1 drugs is the appearance of drug-resistant mutant viruses.
   From November 1996 to December 1998, we examined 1,250 clinical specimens from
329 patients for drug resistance-related mutations. Seventeen hospitals in various
parts of Japan participated in this project. The 329 clinical cases consisted of
210 hemophiliacs infected through contaminated blood products (64%), 55 homosexu-
ally infected patients (17%), 52 heterosexually infected patients (16%), 2 patients
infected through blood transfusion (1%), and 10 patients whose infection route was
unknown. 166 cases received three drugs (50%), 106 cases one or two drugs (32%), 
and 21 cases no drugs; the clinical histories of 36 cases were not known.
   Among the anti-HIV-1 drug-treated patients, 245 patients received AZT (Zidovudine),
134 patients ddI (Didanosine), 101 patients ddC (Zalcitabine), 125 patients d4T 
(Stavudine), 179 patients 3TC (Lamivudine), 81 patients IDV (Indinavir), 38 patients
SQV (Saquinavir), 26 patients RTV (Ritonavir), and 89 patients NFV (Nelfinavir). 
AZT, ddI, d4T, ddC, and 3TC are NRTIs, and IDV, RTV, SQV, and NFV are PIs. 
For determining drug resistance-related mutations, we used the Los Alamos HIV-1 
Drug Resistant Database (3). The data presented below are based on the last data 
obtained for each patient.
   Viral RNAs were extracted from 200ƒÊl plasma by using an RNA purification kit
(Boehringer Mannheim, Indianapolis, IN), and the reverse transcriptase (RT) and 
protease (PR) regions were RT/PCR-amplified in the manner reported previously (4). 
The amplified RT region was 380bp long and the RT region 821 bp long. Sequencing
by the dye-terminator method (5) was conducted by using ABI-377 (Applied Biosystems, 
Foster City, CA) and Sequence Navigator software (Applied Biosystems).
   Figs. 1A and B show the incidence of mutants found in the patients treated with
anti-HIV-1 drugs. Among viruses derived from AZT-treated patients, AZT-specific 
mutation T215Y/E was the most frequent (near 40%), followed by AZT-specific 
mutations M41L, D67N, and K70R. Among viruses derived from 3TC-treated patients,
53% had 3TC-specific mutation M184V. Among viruses derived from PI-treated patients,
mutation L90M for SQV resistance was the most frequent (32%), followed by mutations 
D30N for NFV resistance, G48V for SQV resistance, M46I/L for IDV resistance,
and V82A/F/T for IDV and/or RTV resistance. The mutations occurred only in patients
treated with the respective drugs and never in those treated with other drugs 
(Fig. 1A). Drug resistance to AZT or 3TC was found in 50% of the patients treated 
with the respective drugs. Viruses with mutations related to resistance to ddI or 
d4T were far less frequent (4-6%) (Fig. 1B).
   Fig. 2 shows the incidence of the drug resistant viruses in all specimens 
including those from untreated patients. The resistance to AZT and that to 3TC 
occurred in 38% and 28% of the specimens, respectively. Among the viruses derived
from patients who had not been treated with anti-HIV-drugs, the primary mutations 
were few.  There were no NRTI resistance-related mutations and a very few PI
resistance-related mutations (V82A/F/T for IDV and G48V for SQV in 1%). 
PI resistance-related secondary mutations were more frequent; mutation L10I/R/V 
was found in 2%, K20M/R in 4%, M36I in 9.2%, L63P in 42%, and A71V/T in 9.2%.
   Fig. 3 shows the incidence of viruses classified according to number of drugs
to which the viruses were considered resistant. About half of the viruses had 
mutation(s) for resistance against at least one drug, and one-third had mutations
for resistance against two or more drugs. One case showed resistance even to 
seven drugs (Fig. 3A). Half of the viruses had mutations for resistance against
at least one NRTI, and a quarter had mutations for resistance against two or 
more NRTIs (Fig. 3B). The incidence of mutations related to PI resistance was
lower; 9% of the viruses had mutations for resistance against two or more PIs 
(Fig. 3C). The data as a whole suggested a high prevalence of anti-HIV drug 
resistant mutants among HIV-1s in Japanese patients.

   This study was supported by the Organization for Pharmaceutical Safety and
Research (OPSR) of Japan.


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* Corresponding author: E-mail:wsugiura@nih.go.jp, Fax:+81-42-561-7746 Go to JJID Homepage Go to JJID 52(1)