ABSTRACTThe identification and geographic distribution of the herpes simplex virus type 1 (HSV-1) BglII restriction fragment length polymorphism (RFLP) variants named BgKLand BgOLin clinical isolates from orolabial and cutaneous sites were described in our previous reports, in which the dispersion and replacement of HSV-1 variants were proposed. The base substitution sites deduced from the BgKLmultiple RFLP variations were mapped to the UL12 (DNase), RL2 (α0 transactivator), and latency-associated transcript genes in the present study. The results show that the relative frequencies (RFs) of BgKLare significantly higher in orolabial and cutaneous HSV-1 infections than in ocular infections. For the BgOLvariant, the opposite was found; i.e., the RF of BgOLwas significantly lower in orolabial and cutaneous infections than in ocular infections. No significant differences in the RFs of non-BgKL:non-BgOLisolates were observed. The ratio of the BgKLRF to the BgOLRF was much higher for the orolabial and cutaneous infection groups than for the ocular infection group, whereas the BgKLRF-to-non-BgKL:non-BgOLRF ratios for the former groups were slightly higher than those for the latter group. The higher efficiency of orolabial and cutaneous infections caused by BgKLcompared to the efficiency of infections caused by BgOLallows BgKLto spread more efficiently in human populations and to displace BgOL, because the mouth and lips are the most common HSV-1 infection sites in children. The present study supports our HSV-1 dispersion-and-replacement hypothesis and suggests that HSV-1, the latency-reactivation of which allows variants to accumulate in human populations, has evolved under competitive conditions, providing a new perspective on the polymorphism or variation of HSV-1.

M. tuberculosis strains were isolated from clinically and bacteriologically confirmed patients to evaluate the susceptibility of clinical M. tuberculosis isolates to fluoroquinolone and to obtain molecular epidemiological information in Zambia,. The pathogens were subjected to susceptibility testing with isoniazid, rifampicin, ethambutol and streptomycin. The minimum inhibitory concentrations to ciprofloxacin, sparfloxacin and levofloxacin were also evaluated. The gyrA, fluoroquinolone resistance-determining region (QRDR), was sequenced and analysed. As a result, three of the 16 strains examined were resistant to isoniazid, rifampicin and⁄or streptomycin. All of the strains were susceptible to ciprofloxacin, levofloxacin and sparfloxacin. However, a unique gyrA gene variation of M. tuberculosis was identified in the isolates. One strain had a mutation (T73A) in QRDR. Additionally, 81.25% (13⁄16) of the strains tested had Thr at codon 88. Several variations of gyrA gene have been reported in relation to drug resistance. The gyrA variation data will be useful as epidemiological information. It may be important to monitor fluoroquinolone susceptibility even in developing countries for use against resistant M. tuberculosis infection, even though no fluoroquinolone resistance was observed in this study.

The inappropriate use of anti-tuberculosis drugs has resulted in an increase in the drug resistance. This study was conducted to obtain data related to the spectrum of drug resistant Mycobacterium tuberculosis. A total of 499 strains ofM. tuberculosis were tested for susceptibilities of isoniazid (INH), rifampicin (RFP), ethambutol (EMB) and streptomycin (SM). Totally 225 patients were also evaluated for their clinical manifestations. The primary and acquired resistances were observed in 13.9% and 16.1% to INH, 11.1% and 12.9% to RFP, 6.7% and 9.7% to EMB, and 3.8% and 3.2% to SM respectively. There were no significant differences between primary and acquired resistances. Multi-drug resistance was observed in 22 strains (4.4%). Clinical manifestation, as measured by chest roentgenograms, was similar in patients with either drug-susceptible or resistant strains. The clinical and radiological information was not useful for the prediction of susceptible and resistant strains. The HIV serostatus was not associated with drug susceptibility profiles either. Our study has documented a high incidence of drug resistant M. tuberculosis, with no obvious clinical correlates, which must be considered when implementing a strategy for chemotherapy. As for clinical practices, many defaults during chemotherapy reduced the treatment successes. It is important to assess the efficient implementation of the directly observed treatment with short course chemotherapy (DOTS) and interrupt the further dissemination of resistant M. tuberculosis in the community. The drug resistances must be surveyed continuously to obtain useful clinical perspective and evaluate the effectiveness of tuberculosis control program.

Previous studies of the hemagglutinin (HA) genes of various influenza B virus isolates demonstrated the existence of two antigenically distinct virus lineages represented by B/Victoria/2/87 and B/Yamagata/16/88, respectively. Here, we investigated the antigenic and genetic characteristics of influenza B viruses isolated from children living in Lusaka, Zambia between January and May 1999. Antigenic analysis with chicken antiviral sera showed that all the Zambian isolates had the HA protein belonging to B/Yamagata/16/88-related lineage. Furthermore, phylogenetic analyses of the eight RNA segments performed by using the total or partial nucleotide sequences of the two representative Zambian strains (B/Lusaka/270/99 and B/Lusaka/432/99) as well as the previously reported sequences suggested that the Zambian viruses are closely related to the recently circulating reassortants represented by B/Shiga/T30/98 and B/Yamanashi/166/98 which acquired the genes coding for three polymerase proteins (PB2, PB1, and PA), HA, nucleoprotein, and matrix protein from a B/Yamagata/16/88-like parent and the gene encoding nonstructural proteins (NS1 and NS2) from a B/Guandong/8/93-like parent.

ANNOUNCEMENT2001 AstraZeneca Young Investigator Award RecipientPublished Online:01 Jun 2001https://doi.org/10.1152/ajprenal.2001.280.6.F1115MoreSectionsPDF (101 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInEmail The renal section of the American Physiological Society is pleased to announce that the 2001 recipient of the AstraZeneca Young Investigator Award for excellence in renal physiology is Dr. H. Moo Kwon, Associate Professor of Medicine, Johns Hopkins University. The purpose of this award is to recognize an outstanding young investigator working in any area of renal physiology or hypertension. Dr. Kwon presented his keynote lecture, entitled “How salt regulates genes: function of the transcription factor TonEBP,” at the featured topic session entitled “Hypertonicity stress: new sites of recognition” at the Experimental Biology 2001 meeting in Orlando, FL, March 31-April 4, 2001. Dr. Kwon received his AstraZeneca Young Investigator Award during the renal dinner on Tuesday, April 3, 2001. This award is presented annually at the Experimental Biology meeting and is made possible by the generous support of AstraZeneca, L.P., Wilmington, DE.Download figureDownload PowerPointDr. Kwon received his B.S. degree in Zoology from Seoul National University in South Korea. He then obtained a Ph.D in Renal Physiology in 1987 from the State University of New York at Buffalo. He received postdoctoral training at the Laboratory of Kidney and Electrolyte Metabolism at the National Heart, Lung, and Blood Institute of the National Institutes of Health. He took a position as Instructor in 1990 at Johns Hopkins University in the Nephrology Division and is now an Associate Professor at the same institution. He has published 36 peer-reviewed manuscripts and has written 13 reviews or book chapters.One of the unique features of the renal medulla is its high interstitial salt concentration. Hypertonicity, however, damages DNA and interferes with protein function. Cells adapt to the hypertonicity by accumulating organic osmolytes and upregulating molecular chaperones. During his postdoctoral training, Dr. Kwon and colleagues at the National Institutes of Health and Johns Hopkins University cloned transporters of organic osmolytes (inositol, betaine, and taurine) using Xenopus laevis oocyte expression systems. Because transcription of these genes is stimulated by hypertonicity, subsequent work in his laboratory explored the mechanism by which this occurs. His laboratory observed that an 11-base paircis-element, the tonicity-responsive enhancer (TonE), mediates the transcriptional regulation of the osmolyte transporters and aldose reductase. These investigators went on to clone the transcription factor, TonE binding protein (TonEBP), which mediates this response. Their recent work identified three separate pathways by which TonEBP is activated, i.e. phosphorylation, nuclear localization, and induction through increased transcription. Emerging data show that in the renal medulla TonEBP regulates transporters such as the vasopressin-regulated urea transporter, osmolyte transporters, and aldose reductase. Future research on TonEBP is expected to yield a new paradigm of signal transduction unique to the renal medulla.The APS Renal Section AstraZeneca Young Investigator Award Selection Committee, a subcommittee of the Renal Section Steering Committee, included Susan Wall (Treasurer), Jeff Sands (President), Michael Caplan (Renal Section Program Committee), and Christine Baylis (Renal Section Program Committee). The Renal Section wishes to express its sincere appreciation to the Scientific Commercialization Skill Center (SCSC) of AstraZeneca, L.P., for its generous support of biomedical education.This article has no references to display. Previous Back to Top Next FiguresReferencesRelatedInformationCited ByTranslational Modeling of Chloroquine and Hydroxychloroquine Dosimetry in Human Airways for Treating Viral Respiratory Infections9 January 2022 | Pharmaceutical Research, Vol. 39, No. 1Kakkonto Inhibits Cytokine Production Induced by Rhinovirus Infection in Primary Cultures of Human Nasal Epithelial Cells31 August 2021 | Frontiers in Pharmacology, Vol. 12 More from this issue > Volume 280Issue 6June 2001Pages F1115-F1115 Copyright & PermissionsCopyright © 2001 the American Physiological Societyhttps://doi.org/10.1152/ajprenal.2001.280.6.F1115PubMed11350790History Published online 1 June 2001 Published in print 1 June 2001 PDF download Metrics Downloaded 281 times

Previously, it was demonstrated that any human immunodeficiency virus type 1 (HIV-1) strain proliferating in peripheral blood mononuclear cells (PBMCs) in vitro, and resuspended in seronegative plasma, could be captured efficiently (mean > 95%) by a porous polypropylene (PP) membrane modified cationically. We investigated if this cationic membrane could capture HIV-1 obtained from seropositive plasma, and confirmed whether this membrane was effective for the preparation of safe plasma products against HIV-1 transmission. Thirty-six seropositive plasma samples derived from HIV-1 positive cohorts in New York and Lusaka (Republic of Zambia), including 18 cases of acquired immunodeficiency syndrome (AIDS) related complex, AIDS and five terminal cases of AIDS, were filtered through the cationic membrane to determine the reduction of RNA concentration, the gag p24 concentration, and infectious titer. Only a small reduction in RNA concentration (mean < 20%) and almost no decrease in gag concentration (mean < 2%) were obtained, despite the fact that the infectivity was eliminated entirely by the filtration. Due to the possibility that anti-HIV-1 antibodies in patients' plasma combine with HIV-1, laboratory-adapted HIV-1(HTLV-IIIB) was mixed with seropositive plasma to test the effect of antibodies on HIV-1 adsorption, and also to investigate the interfacial electrokinetic potential (zeta-potential) of both intact and plasma-treated HIV-1. The zeta-potential of HIV-1(HTLV-IIIB) in the presence of seropositive plasma was neutral as opposed to negative when stored in seronegative plasma or culture medium. Also the rate of HIV-1 capture by the membrane, as determined by the reduction in RNA concentration, sank from 95% to 20%, the same capture percentage observed when filtering plasma of patients. These findings suggested that in patients' plasma, the antibody-masked HIV-1 comprise most of the viral population, and was not trapped on the cationic membrane because of its electrostatic character. Conversely, the cationic membrane was thought to adsorb antibody-free HIV-1 exclusively. It was suggested that each viral swarm had its own zeta-potential, and this difference in electrostatic character determined the extent of the viral adsorption by the cationic membrane.

To examine the effects of bafilomycin A(1), a blocker of vacuolar H(+)-ATPase, on rhinovirus (RV) infection in the airway epithelium, primary cultures of human tracheal epithelial cells were infected with RV14. Viral infection was confirmed by showing that viral RNA in the infected cells and the viral titers in the supernatants of infected cells increased with time. RV14 infection upregulated the production of cytokines and mRNA of intercellular adhesion molecule (ICAM)-1 in epithelial cells. Bafilomycin A(1) reduced the viral titers of RV14 and inhibited the production of cytokines and ICAM-1 before and after RV14 infection. Bafilomycin A(1) reduced susceptibility of epithelial cells to RV14 infection. RV14 increased activated nuclear factor-kappaB in the cells, and bafilomycin A(1) reduced the activated nuclear factor-kappaB. Bafilomycin A(1) decreased the number of acidic endosomes in the epithelial cells. These results suggest that bafilomycin A(1) may inhibit infection by RV14 by not only blocking RV RNA entry into the endosomes but also reducing ICAM-1 expression in the epithelial cells. Bafilomycin A(1) may therefore modulate airway inflammation after RV infection.

To examine the effects of glucocorticoid on rhinovirus (RV) infection, primary cultures of human tracheal epithelial cells were infected with either RV2 or RV14. Viral infection was confirmed by demonstrating that viral RNA in infected cells and viral titers of supernatants and lysates from infected cells increased with time. RV14 infection upregulated the expression of mRNA and protein of intercellular adhesion molecule-1 (ICAM-1), the major RV receptor, on epithelial cells, and it increased the production of interleukin (IL)-1beta, IL-6, IL-8, and tumor necrosis factor-alpha in supernatants. Dexamethasone reduced the viral titers of supernatants and cell lysates, viral RNA of infected cells, and susceptibility of RV14 infection in association with inhibition of cytokine production and ICAM-1 induction. In contrast to RV14 infection, dexamethasone did not alter RV2 infection, a minor group of RVs. These results suggest that dexamethasone may inhibit RV14 infection by reducing the surface expression of ICAM-1 in cultured human tracheal epithelial cells. Glucocorticoid may modulate airway inflammation via reducing the production of proinflammatory cytokines and ICAM-1 induced by rhinovirus infection.

To further understand the early biochemical events that occur in infected surface epithelium, we developed for the first time a model in which a respiratory submucosal gland cell population can be infected with rhinovirus (RV). Viral infection was confirmed by demonstrating with PCR that viral titers in supernatants and lysates from infected cells increased with time. Infection by RV14 upregulated the expression of intercellular adhesion molecule-1 (ICAM-1) mRNA, the major RV receptor, on submucosal gland cells, and it increased production of interleukin (IL)-1α, IL-1β, IL-6, IL-8, tumor necrosis factor-α, and granulocyte-macrophage colony-stimulating factor in supernatants. Antibodies to ICAM-1 inhibited RV infection of submucosal gland cells and decreased the production of cytokines after RV infection. Both IL-1α and IL-1β upregulated ICAM-1 mRNA expression and increased susceptibility to RV infection, whereas other cytokines failed to alter ICAM-1 mRNA expression. Furthermore, neutralizing antibodies to IL-1α and IL-1β significantly decreased the viral titers in supernatants and ICAM-1 mRNA expression after RV infection, but a neutralizing antibody to tumor necrosis factor-α was without effect. These findings suggest that respiratory submucosal gland cells play an important role in the initial stages of inflammation and provide useful insights into the pathogenesis of RV infection.

The study was carried out to evaluate the therapeutic effects of zanamivir, a highly selective, potent and specific inhibitor of influenza A and B virus neuraminidases, in adult patients with acute influenzalike illness. Patients who presented within 36 h of the onset of influenza-like symptoms were randomly assigned to receive one of three treatments, twice daily, for 5 days: 10 mg zanamivir powder for inhalation (zanamivir inhalation group), 10 mg zanamivir powder for inhalation plus 6.4 mg zanamivir nasal spray (zanamivir inhalation plus intranasal group) or placebo (placebo group). The primary end point was the time to alleviation of the three major symptoms (fever, headache and myalgia). The secondary end point was the time to alleviation of five influenza symptoms (fever, headache, myalgia, cough and sore throat). One hundred and sixteen patients with influenza-like illness were recruited to the study. No differences were observed between the two groups of patients who received zanamivir (inhalation group or inhalation plus intranasal group). Patients who received zanamivir recovered significantly faster (median 3 days to recovery) than the patients in the placebo group (median 4 days to recovery; P < 0.01). Topically administered zanamivir was well tolerated. This study confirms that in adults, topically administered zanamivir is well tolerated and is effective in reducing the time to alleviation of influenza symptoms.

Epidemiological research on respiratory syncytial virus (RSV) infections in children was carried out at the Virology Laboratory, University Teaching Hospital (UTH), in Lusaka, Zambia, from January–December 1996. Specimens including 736 nasal washings and 2424 throat swabs were collected from children with acute respiratory infections (ARI) and tested for RSV by enzyme immunoassay and by virus isolation. RSV was isolated in 62 (4·1%) of 1496 throat swabs collected from March to September and was detected in 99 (16·3%) of 609 nasal washings from March to November. The average RSV isolation rate was 2·6% and the average RSV detection rate was 13·5%. The highest RSV isolation (8·1%) and detection (30·5%) rates were in June 1996. RSV antibody in the 278 serum specimens collected from Zambian children, who were hospitalized in the paediatric ward, UTH, was detected using a standard neutralization test. The antibody positive rate was 60–80% in children >4 years. It is evident that RSV is one of the main causal agents of ARI in children in Zambia.

The antigenic and genetic characteristics of the 18 human strains of influenza C virus isolated in Yamagata and Sendai Cities, Japan between January 1991 and February 1993 were investigated. Antigenic analysis with monoclonal antibodies to the hemagglutinin-esterase glycoprotein showed that the isolates could be divided into three distinct groups closely related to C/Yamagata/26/81, C/Aichi/1/81 and C/Mississippi/80, respectively. T1-oligonucleotide fingerprinting of total vRNA revealed that the six isolates belonging to the C.Yamagata/26/81 virus group had the genomes greatly similar to one another but considerably different from those of the 1988/1990 isolates (except C/Yamagata/10/89) of the same antigenic group. Comparison of total or partial nucleotide sequences of the seven RNA segments of the three strains (C/Miyagi/3/91, C/Miyagi/9/91 and C/Miyagi/2/92) representative of the 1991/1993 strains of the C/Yamagata/26/81 virus group with those of the previous influenza C isolates obtained from humans and pigs during 1980/1989 showed that the 1991/1993 strains, like C/Yamagata/10/89, are more closely related to viruses isolated from pigs in Beijing, China in 1981/1982 than to any of the isolates from humans. This observation suggests strongly that interspecies transmission of influenza C virus between humans and pigs has occurred in nature, although it is not known whether the virus has been transmitted from pigs to humans or from humans to pigs.

Exacerbations of asthma are often associated with respiratory infection caused by rhinoviruses. To study the effects of rhinovirus infection on respiratory epithelium, a primary target for respiratory viruses, human rhinovirus (HRV)-2 and HRV-14 were infected to primary cultures of human tracheal epithelial cells. Viral infection was confirmed by showing that viral titers of supernatants and lysates from infected cells increased with time and by polymerase chain reaction. HRV-2 and HRV-14 infections upregulated the expression of intercellular adhesion molecule-1 (ICAM-1) mRNA, the major rhinovirus receptor, on epithelial cells, and they increased the production of interleukin (IL)-1β, IL-6, IL-8, and tumor necrosis factor (TNF)-α in supernatants. Antibodies to ICAM-1 inhibited HRV-14 infection of epithelial cells and decreased the production of cytokines after HRV-14 infection, but they did not alter HRV-2 infection-induced production of cytokines. IL-1β upregulated ICAM-1 mRNA expression and increased susceptibility to HRV-14 infection, whereas other cytokines failed to alter ICAM-1 mRNA expression. Furthermore, a neutralizing antibody to IL-1β significantly decreased viral titers of supernatants and ICAM-1 mRNA expression after HRV-14 infection, but a neutralizing antibody to TNF-α was without effect. Immunohistochemical studies revealed that both HRV-14 infection and IL-1β increased ICAM-1 expression on cultured epithelial cells. These findings imply that HRV-14 infection upregulated ICAM-1 expression on epithelial cells through increased production of IL-1β, thereby increasing susceptibility to infection. These events may be important for amplification of airway inflammation after viral infection in asthma.

A viral aetiological and epidemiological study of acute respiratory infections (ARI) in children was carried out in Lusaka, Zambia between June 1993 and September 1995. A total of 3,760 throat swab specimens were collected for virus isolation from children under 5 years of age who had ARI and were attending three health centres in Lusaka. Between June and November 1993, 52 cases of the influenza A/H3N2 viruses were isolated. Between May and July 1994, 34 influenza B cases were isolated. In 1995, one A/H3N2 influenza virus was isolated in January and then the same type of influenza virus was isolated from 55 samples between June and August. The isolation rate of influenza virus was highest at 14.3% (20/139) in August 1993, at 15.1% (18/119) in June 1994 and at 25.4% (43/169) in July 1995. This is the first report of a consecutive study of influenza virus infections in Zambia and the results reveal that influenza virus infections are one of the most important pathogens of ARI in children in the cool, dry season (June-August) in this country.

The Associated Press reports that on October 2 Indian Prime Minister Inder Kumar Gujral initiated a program to give 500 rupees ($14 U.S. +/-) to very poor families after the birth of a daughter. The Prime Minister's intent is to counteract the cultural factors that he says compel some Indian families to discriminate against, and in some cases even murder, their female infants. How the government will identify families that qualify for the cash, and then distribute it, has yet to be determined.

Laboratory diagnosis of measles infection is rarely performed in developing countries and tends to depend on clinical symptoms alone. We evaluated detection of immunoglobulin M (IgM) antibodies for confirmation of acute measles infection in Zambia. In 149 hospitalized children with clinical diagnosis of measles, IgM antibodies were detected in 88.6% (132/149). The IgM‐positive rate increased with time after onset of skin rash and all samples were positive after 4 days. In addition to IgM antibody test, virus isolations from throat swabs using B95a cells were also performed. These were positive in only 20.9% (14/67), and both IgM and virus isolation in combination increased the positive rate to 92.5% (62/67). Vaccinated children had higher neutralizing (Nt) antibody responses and, among IgM‐negative patients, all 4 vaccinated children had high Nt antibodies while all 10 unvaccinated children had negative or low Nt results. The IgM antibody test was proved to be a sensitive method for laboratory confirmation of measles virus infection in developing countries.

Previous studies of the haemagglutinin-esterase (HE) genes of various influenza C isolates suggested the existence of three distinct virus lineages (C/Yamagata/26/81-, C/Aichi/1/81- and C/Mississippi/80-related lineages) in Japan in the 1980s. Here we analysed the genetic properties of three strains (C/Yamagata/5/92, C/Miyagi/3/93 and C/Miyagi/4/93) isolated in Yamagata and Sendai Cities, Japan, in 1992/1993. Comparison of total or partial nucleotide sequences of the seven RNA segments of C/Yamagata/5/92 with those of 11 previous isolates suggested that the 1992 strain is a reassortant which inherited HE, P3, NP and M genes from a C/Mississippi/80-like virus and PB2, PB1 and NS genes from a C/pig/Beijing/115/81-like virus. Furthermore, it became evident that at least two (C/England/83 and C/Yamagata/9/88) of the 11 reference strains are also reassortants.

The etiology of acute lower respiratory tract infections (ALRI) was studied in pediatric inpatients under 2 years of age admitted to Chiba Municipal Hospital between June 1994 and March 1995. Eighty-seven patients, 99 episodes were investigated for bacterial infection with the use of blood culture and washed sputum culture, for viral infection with the use of virus isolation, antigen detection and antibody assays, for Mycoplasma pneumoniae infection with the use of antibody assay and for Chlamydia infection with the use of antigen detection. Pathogens were identified in 71 (71%) of the 99 episodes. Evidence of bacterial infection was detected in 43 episodes (43%), viral infection in 37 episodes (37%), Mycoplasma pneumoniae infection in 4 episodes (4%) and Chlamydia infection 3 episodes (3%). The major bacterial pathogens were H. influenzae, M. (B) catarrhalis and S. pneumoniae. RS virus and influenza virus epidemics occurred during the winter. A mixed bacterial and viral infection was documented in 13 episodes (13%). RS virus infection was common in infants up to 6 months old. Mixed bacterial and influenza virus infections were common in 1 or more year old children. Virus isolation was useful for the grasp of the viral epidemic. Bacterial associated infections were common in children under 2 years of age with ALRI. Washed sputum culture and sputum gram stains' were useful for the treatment of infant ALRI.

Measles is known to be more severe in human immunodeficiency virus (HIV-1)-infected children. 1 Kaplan LJ Daum RS Smaron M McCarthy Severe measles in immunocompromized patients. JAMA. 1992; 267: 1237-1241 Crossref PubMed Scopus (293) Google Scholar In sub-Saharan Africa, measles is still a major cause of morbidity and mortality in infants and children, and HIV-1 infection is increasing rapidly in this age group. Measles prevention in HIV-infected children is an important public health issue. Measles vaccine has been shown to be immunogenic and not associated with increased severe acute adverse reactions in HIV-infected children, 2 Cutts FT Mandala K St Louis M et al. Immunogenicity of high-titer Edmonton-Zagreb measles vaccine in human immunodeficiency virus-infected children in Kinshasa, Zaire. J Infect Dis. 1993; 167: 1418-1421 Crossref PubMed Scopus (26) Google Scholar and its use has been recommended by WHO. 3 Global Program on AIDS and Expanded Program on Immunization Joint WHO/UNICEF statement on early immunization for HIV-infected children. MMWR Wkly Epidemiol Rec. 1989; 64: 48-49 Google Scholar However, long-term protective efficacy and safety of measles vaccine in HIV-infected African children is unknown.

Journal Article Prevalence of hepatitis B antigens in human immunodeficiency virus type 1 seropositive and seronegative pregnant women in Zambia Get access H. Oshitani, H. Oshitani ∗ 1Virus Research Centre, Sendai National Hospital, Sendai, Japan ∗Address for correspondence: H. Oshitani, MD, Sendai National Hospital, Virus Research Centre, 2-8-8 Miyagino-ku, Sendai, 983, Japan; fax +81 22 291 8114. Search for other works by this author on: Oxford Academic PubMed Google Scholar F.C. Kasolo, F.C. Kasolo 2Virology Laboratory, University Teaching Hospital, Lusaka, Zambia Search for other works by this author on: Oxford Academic PubMed Google Scholar M. Mpabalwani, M. Mpabalwani 2Virology Laboratory, University Teaching Hospital, Lusaka, Zambia Search for other works by this author on: Oxford Academic PubMed Google Scholar K. Mizuta, K. Mizuta 2Virology Laboratory, University Teaching Hospital, Lusaka, Zambia Search for other works by this author on: Oxford Academic PubMed Google Scholar N.P. Luo, N.P. Luo 2Virology Laboratory, University Teaching Hospital, Lusaka, Zambia Search for other works by this author on: Oxford Academic PubMed Google Scholar H. Suzuki, H. Suzuki 1Virus Research Centre, Sendai National Hospital, Sendai, Japan Search for other works by this author on: Oxford Academic PubMed Google Scholar Y. Numazaki Y. Numazaki 1Virus Research Centre, Sendai National Hospital, Sendai, Japan Search for other works by this author on: Oxford Academic PubMed Google Scholar Transactions of The Royal Society of Tropical Medicine and Hygiene, Volume 90, Issue 3, May-June 1996, Pages 235–236, https://doi.org/10.1016/S0035-9203(96)90227-8 Published: 01 June 1996 Article history Received: 30 August 1995 Revision received: 12 December 1995 Accepted: 02 January 1996 Published: 01 June 1996