NICD Science Focus

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Science Focus
Issue 1 — November 2013
A bi-monthly newsletter that acknowledges NICD staffers who have published in peer reviewed journals.The Science Focus is a
quarterly compilation of the scientific publications included in the quarterly report submitted to the National Department of
Health and includes only publications where an NICD staff member is either the first or the last author.
A DIMORPHIC FUNGUS CAUSING DISSEMINATED INFECTION IN SOUTH AFRICA
Kenyon C, Bonorchis K, Corcocan C, Meintjes G, Locketz M, Lehloenya R, Vismer HF, Naicker P, Prozesky H,
van Wyk M, Bamford C, du Plooy M, Imrie G, Dlamini S, Borman AM, Colebunders R, Yansouni CP, Mendelson
M, Govender NP
Govender NP
The genus Emmonsia contains three species that are associated with human
disease. Emmonsia crescens and Emmonsia parva are the agents that cause
adiaspiromycosis, and one human case of Emmonsia pasteuriana infection has been described. We report a
fungal pathogen within the genus Emmonsia that is most closely related to E. pasteuriana in
human immunodeficiency virus (HIV)-infected adults in South Africa. Between July 2008 and July 2011, we
conducted enhanced surveillance to identify the cause of systemic, dimorphic fungal infections in patients
presenting to Groote Schuur Hospital and other hospitals affiliated with the University of Cape Town, Cape
Town, South Africa. DNA sequencing was used to identify pathogenic fungi. A total of 24 cases of dimorphic
fungal infection were diagnosed, 13 of which were caused by an Emmonsia species. All 13 patients were
HIV-infected, with a median CD4+ T-cell count of 16 cells per cubic millimeter (interquartile range, 10 to 44),
and all had evidence of disseminated fungal disease. Three patients died soon after presentation, but the
others had a good response to a variety of antifungal agents and antiretroviral therapy. Phylogenetic analysis
of five genes (LSU, ITS1-2, and the genes encoding actin, β-tubulin, and intein PRP8) revealed that this
fungus belongs in the genus Emmonsia and is most closely related to E. pasteuriana. The findings suggest
that these isolates of an Emmonsia species represent a new species of dimorphic fungus that is pathogenic
to humans. The species appears to be an important cause of infections in Cape Town.
Impact factor: 51.658
VIRAL ESCAPE FROM HIV-1 NEUTRALIZING ANTIBODIES DRIVES INCREASED PLASMA NEUTRALIZING BREADTH THROUGH SEQUENTIAL RECOGNITION OF MULTIPLE EPITOPES AND IMMUNOTYPES
Wibmer CK, Bhiman JN, Gray ES, Tumba N, Abdool Karim SS, Williamson C, Morris L, Moore PL
Identifying the targets of broadly neutralizing antibodies to HIV-1 and
understanding how these antibodies develop remain important goals in the quest
to rationally develop an HIV-1 vaccine. We previously identified a participant in
Wibmer CK
the CAPRISA Acute Infection Cohort (CAP257) whose plasma neutralized 84%
of heterologous viruses. In this study we showed that breadth in CAP257 was largely due to the sequential,
transient appearance of three distinct broadly neutralizing antibody specificities spanning the first 4.5 years
of infection. The first specificity targeted an epitope in the V2 region of gp120 that was also recognized by
strain-specific antibodies 7 weeks earlier. Specificity for the autologous virus was determined largely by a
rare N167 antigenic variant of V2, with viral escape to the more common D167 immunotype coinciding with
the development of the first wave of broadly neutralizing antibodies. Escape from these broadly neutralizing
V2 antibodies through deletion of the glycan at N160 was associated with exposure of an epitope in the
CD4 binding site that became the target for a second wave of broadly neutralizing antibodies. Neutralization
by these CD4 binding site antibodies was almost entirely dependent on the glycan at position N276. Early
viral escape mutations in the CD4 binding site drove an increase in wave two neutralization breadth, as this
second wave of heterologous neutralization matured to recognize multiple immunotypes within this site.
Altogether this study showed that the human immune system is capable of generating multiple broadly
neutralizing antibodies in response to a constantly evolving viral population that exposes new targets as a
consequence of escape from earlier neutralizing antibodies.
Impact factor: 8.14
1
HIV AND INFLUENZA INFECTION ARE ASSOCIATED WITH INCREASED BLOOD PNEUMOCOCCAL
LOAD,SOUTH AFRICA,2009-2011
Wolter N, Cohen C, Tempia S, Madhi SA, Venter M, Moyes J, Walaza S, Kgokong BM, Groome M, du
Plessis M, Pretorius M, Dawood H, Kahn K, Variava E, Klugman KP, von Gottberg A
Increased pneumococcal loads are associated with severe outcomes.
We determined the prevalence of pneumococcal DNA in blood
specimens from patients hospitalized with acute lower respiratory tract
infection and identified factors associated with invasive pneumococcal pneumonia, bacterial loads,
and death. Methods. A total of 8523 patients were enrolled as part of prospective hospital-based
surveillance. Blood was collected for quantitative pneumococcal (lytA) detection, and
nasopharyngeal specimens were collected for detection of influenza virus and other respiratory
viruses by real-time polymerase chain reaction. Results. Of 6396 cases (75%) with lytA results, 422
(7%) were positive for pneumococcal DNA. The prevalences of human immunodeficiency virus
(HIV) and influenza virus were 51% (2965/5855) and 8% (485/6358), respectively. On multivariable
analysis, HIV infection (adjusted odds ratio [aOR], 2.4; 95% confidence interval [CI], 1.6-3.6),
influenza virus coinfection (aOR, 1.4; 95% CI, 1.2-2.1), oxygen therapy during admission (aOR, 1.6;
95% CI, 1.1-2.3) and in-hospital death (aOR, 2.1; 95% CI, 1.1-4.0) were significantly associated with
increased pneumococcal load. Among lytA-positive patients, after adjustment for length of
hospitalization, duration of symptoms, and oxygen therapy during admission, pneumococcal loads
≥10,000 DNA copies/mL (aOR, 3.6; 95% CI, 1.8-7.2) were associated with increased risk of death.
Conclusions. HIV and influenza virus infections were associated with elevated pneumococcal
loads, which, in turn, were associated with increased risk of death.
Wolter N
Impact factor: 5.848
GENETIC CHARACTERIZATION OF HERPES SIMPLEX VIRUS TYPE 2 UL23 THYMIDINE KINASE IN JOHANNESBURG,SOUTH AFRICA
Müller EE, Magooa MP, Lewis DA
Müller EE
Herpes simplex virus type 2 (HSV-2) is currently the leading cause of
Genital Ulcer Disease (GUD) both globally and within South Africa. HSV-2 infections are most often
treated with acyclovir (ACV), a guanosine nucleoside analogue that requires phosphorylation by virus
-encoded thymidine kinase (TK). Resistance to ACV is mainly due to mutations in the viral UL23
gene that codes for TK. ACV was added as part of the first-line syndromic management treatment
algorithm for GUD in South Africa in late 2008. In order to assess the prevalence of TK-associated
ACV resistance among HSV-2 virions detected in genital ulcer specimens, pre- and post-introduction
of ACV, we amplified and fully sequenced the UL23 gene of 254 HSV-2 positive specimens obtained
from participants in GUD aetiological surveys conducted between 2007 and 2011 in Johannesburg,
South Africa. We identified 63 nucleotide mutations in the UL23 genes analysed, that resulted in 30
silent mutations and 32 amino acid changes. A large proportion (41%) of these amino acid changes
were due to previously described natural polymorphisms that occur in both sensitive and resistant
HSV strains. In addition, we identified 19 unknown amino acid changes in 30 samples that have not
been described before. All mutations detected were outside the recognised TK conserved domains
where ACV resistance mutations typically occur. No frameshift mutations or mutations causing stop
codons were identified in those UL23 genes analysed. Importantly, no evidence was found of known
ACV resistance mutations in HSV-2 following the addition of ACV as first-line therapy for GUD.
Impact factor: 3.685
2
PROSPECTIVE COHORT STUDY COMPARING SEASONAL AND H1N1 (2009) PANDEMIC
INFLUENZA VIRUS ILLNESSES IN HIV INFECTED CHILDREN DURING 2009
Madhi SA, Kuwanda L,Venter M, Violari A
Madhi SA
A cohort of 410 young HIV-infected children was prospectively investigated for seasonal and A
(H1N1p)2009 influenza virus illness during 2009. The incidence of confirmed illness due to
seasonal influenza was three-fold greater than A(H1N1p)2009 (0.7 vs. 0.2 per 100 child-weeks,
respectively; p=0.0001) and the clinical presentations were similar. Illnesses due to seasonal and
A(H1N1p)2009 influenza were self-limiting without neuraminidase inhibitor therapy.
Impact factor: 3.569
EPIDEMIOLOGY OF INVASIVE PNEUMOCOCCAL DISEASE IN THE PRE-CONJUGATE
VACCINE-ERA: SOUTH AFRICA,2003-2008
von Gottberg A, Cohen C, de Gouveia L, Meiring S, Quan V, Whitelaw A, Crowther-Gibson P,
Madhi SA, Whitney CG, Klugman KP
von Gottberg A
Dynamics of pneumococcal disease incidence and serotype distribution
prior to introduction of pneumococcal conjugate vaccines (PCV) will
assist in understanding effects of the vaccine over time and will be important in choosing the optimal
PCV formulation.We conducted active, laboratory-based, national surveillance for invasive
pneumococcal disease (IPD) through the Group for Enteric, Respiratory and Meningeal Disease
Surveillance in South Africa (GERMS-SA) from 2003 through 2008. Over 130 laboratories report to
this system. Pneumococci were serotyped using Quellung and isolates screened for resistance by disk
diffusion; minimum inhibitory concentrations were determined on potentially resistant isolates. We
used univariate and multivariable multinomial regression models to assess differences between
serotypes.GERMS-SA identified 8674 cases among children <5 years. Overall, 58% (3849/6668), 65%
(4314/6668), and 85% (5669/6668) of cases and 61% (455/751), 64% (482/751), 82% (616/751) of
deaths were due to serotypes included in 7-valent PCV, 10-valent PCV and 13-valent PCV,
respectively. Serotypes 6A and 19A accounted for 16% (527/3252) of penicillin non-susceptible
disease. In 2008, reported incidence of IPD was 6-fold higher in children <1 compared to children 1-4
years of age: 87 per 100,000 population and 14/100,000, respectively. The relative risk of IPD was
21-fold (95% CI, 19-24) and 34-fold (29-41) greater in HIV-infected compared to HIV-uninfected
children in the <1 year and 1-4-year-old age groups respectively. On multivariable analysis serotypes
6B (relative risk ratio (RRR) 0.7; confidence interval (CI) 0.5-0.9), 18C (RRR 0.3; CI 0.1-0.5), 1 (RRR
0.2; CI 0.1-0.4) and 8 (RRR 0.2; CI 0.1-0.4) were significantly less common in HIV-infected individuals
than serotype 14. All vaccine formulations have the potential to prevent most cases and deaths from
IPD in children in South Africa. Vaccines with protection against 19A would be advantageous in South
Africa.
Impact factor: 3.492
3
INACTIVATED WEST NILE VIRUS (WNV) VACCINE, DUVAXYN WNV, PROTECTS AGAINST A HIGHLY
NEUROINVASIVE LINEAGE 2 WNV STRAIN IN MICE
Venter M, van Vuren PJ, Mentoor J, Paweska J, Williams J
Lineage 2 West Nile Virus (WNV) is endemic to southern Africa and
Madagascar, and has recently been associated with encephalitis
outbreaks in humans and horses in South Africa, central Europe, Italy
Venter M
and Greece. Commercial vaccines have mostly been evaluated against
WNV lineage 1 strains and their efficacy against lineage 2 strains rarely reported. To evaluate
protection of Duvaxyn WNV vaccine against lineage 2 strains associated with encephalitis in
South Africa, mice were vaccinated twice intramuscularly three weeks apart, and challenged four
weeks later with highly neuroinvasive lineage 1 strain NY385/99 or lineage 2 strain SPU93/01.
Neutralising antibody titres were measured at the time of challenge and three weeks later.
Immunohistochemistry and reverse transcription polymerase chain reaction (RT-PCR) were
conducted on brains of mice that succumbed during the trial, on controls and on vaccinated mice
that survived. Serum neutralising antibodies in vaccinated mice were detected but low three weeks
after primovaccination. Three weeks post-challenge, vaccinated mice had significantly higher
serum neutralising antibody titres against both lineages than unvaccinated controls. After
challenge, all vaccinated mice remained healthy but all unvaccinated mice demonstrated severe
neurological signs with 75% mortality rate. WNV was not detected in brains of vaccinated mice
whereas virus replicated in most unvaccinated mice challenged with either lineage. Gross and
microscopic lesions were found only in unvaccinated mice challenged with both lineages.
Duvaxyn WNV vaccine provided complete protection against challenge with lineage 2 WNV and
stimulated significant cross protective neutralising antibodies in mice against lineage 2.
Impact factor: 3.492
MECHANISMS OF HIV-1 SUBTYPE C RESISTANCE TO GRFT,CV-N AND SVN
Alexandre K, Moore PL,Nonyane M, Gray ES,Ranchobe R, Chakauya E, McMahon J, O’Keefe B,
Chikwamba R, Morris L
Alexandre K
We examined the ability of HIV-1 subtype C to develop resistance to the inhibitory lectins, griffithsin
(GRFT), cyanovirin-N (CV-N) and scytovirin (SVN), which bind multiple mannose-rich glycans on gp120.
Four primary HIV-1 strains cultured under escalating concentrations of these lectins became
increasingly resistant tolerating 2 to 12 times their 50% inhibitory concentrations. Sequence analysis of
gp120 showed that most had deletions of 1 to 5 mannose-rich glycans. Glycosylation sites at positions 230,
234, 241, 289 located in the C2 region and 339, 392 and 448 in the C3-C4 region were affected. Furthermore, deletions and insertions of up to 5 amino acids in the V4 region were observed in 3 of the 4 isolates.
These data suggest that loss of glycosylation sites on gp120 as well as rearrangement of glycans in V4
are mechanisms involved in HIV-1 subtype C escape from GRFT, CV-N and SVN.
Impact factor:3.367
4
TRENDS AND ASSOCIATIONS OF TRICHOMONAS VAGINALIS INFECTION IN MEN AND
WOMEN WITH GENITAL DISCHARGE SYNDROMES IN JOHANNESBURG,SOUTH AFRICA
Lewis DA, Marsh K, Radebe F, Maseko V, Hughes G
Lewis DA
To better understand the epidemiology of Trichomonas vaginalis infection, we
investigated the association between T vaginalis and demographic, clinical,
microbiological and behavioural characteristics of patients presenting with genital
discharges to a primary healthcare clinic in Johannesburg, South Africa. During six
annual surveys (2007-2012), 1218 cases of male urethral discharge syndrome and
1232 cases of vaginal discharge syndrome were consecutively recruited.
Diagnostic methods included nucleic acid amplification (Neisseria gonorrhoeae,
Chlamydia trachomatis, T vaginalis and Mycoplasma genitalium), microscopy
(bacterial vaginosis and Candida) and serology (Treponema pallidum, herpes
simplex virus type 2 (HSV-2) and HIV). Logistic regression analyses and χ2 tests
were used to identify predictors of T vaginalis infection. The prevalence of T
vaginalis decreased from 2007 to 2012 (men from 13.4% to 4.8%; women from
33.8 to 23.1%). Overall, 74 (6.1%) men and 291 (23.6%) women were T vaginalis
positive, with the highest prevalence in those aged ≥40 years (men 13.6%; women
30.9%). T vaginalis infection occurred more often in pregnant women (adjusted OR
(aOR) 2.67; 95% CI 1.29 to 5.54) and in women with serological evidence of T
pallidum (aOR 1.63; 95% CI 1.08 to 2.45) or HSV-2 infections (aOR 1.75; 95% CI
1.16 to 2.64). T vaginalis infection occurred less often in men with coexistent
gonorrhoea (aOR 0.35; 95% CI 0.21 to 0.57) and in women with either bacterial
vaginosis (aOR 0.60; 95% CI 0.44 to 0.82) or Candida morphotypes (OR 0.61;
95% CI 0.43 to 0.86). Although the prevalence of T vaginalis infection has decreased over time, it remains an important cause of genital discharge in South
Africa, particularly in older patients and pregnant women.
Impact factor: 2.611
5
FIRST INSIGHTS INTO SPECIES AND GENOTYPES OF ECHINOCOCCUS IN SOUTH AFRICA
Mogoye BK, Menezes CN, Wong ML, Stacey S, von Delft D, Wahlers K, Wassermann M, Romig T,
Kern P, Grobusch MP, Frean J
Frean J
Cystic echinococcosis is a serious and neglected parasitic zoonosis that is
regarded as an emerging disease world-wide. Effective control of the disease is based on understanding the variability of Echinococcus granulosus (sensu lato), as genotypic characteristics may influence lifecycle patterns, development rate, and transmission. No molecular epidemiological research
has previously been conducted to shed light on genotypes responsible for the disease in South Africa. To identify strains circulating in the country, parasite material was collected from patients between
August 2010 and September 2012 and analyzed by PCR/RFLP methods. A total of 32 samples was
characterized as E. granulosus sensu stricto (G1-G3) (81%), E. canadensis (G6/7) (16%) and E.
ortleppi (G5) (3%). Furthermore, two co-amplifying G6/7 genotypes were confirmed as G7 by sequencing. This is the first report on genotyping of Echinococcus species in South Africa, and, to the
best of our knowledge, the first report of the G5 and G7 genotypes from humans in Africa.
Impact factor: 2.381
DEVELOPMENT OF A RIFT VALLEY FEVER REAL-TIME RT-PCR ASSAY THAT CAN DETECT
ALL THREE GENOME SEGMENTS
Wilson WC, Romito M, Jasperson DC, Weingartl H, Binepal YS, Maluleke MR, Wallace DB, van Vuren
PJ, Paweska JT
Paweska JT
Outbreaks of Rift Valley fever in Kenya, Madagascar, Mauritania, and South Africa had devastating
effects on livestock and human health. In addition, this disease is a food security issue for endemic
countries. There is growing concern for the potential introduction of RVF into non-endemic countries. A
number of single-gene target amplification assays have been developed for the rapid detection of RVF
viral RNA. This paper describes the development of an improved amplification assay that includes
two confirmatory target RNA segments (L and M) and a third target gene, NSs, which is deleted in the
Clone 13 commercial vaccine and other candidate vaccines. The assay also contains an exogenous
RNA control added during the PCR setup for detection of amplification inhibitors. The assay was
evaluated initially with samples from experimentally infected animals, after which clinical veterinary and
human samples from endemic countries were tested for further evaluation. The assay has a sensitivity
range of 66.7-100% and a specificity of 92.0-100% depending on the comparison. The assay has an
overall sensitivity of 92.5%, specificity of 95% and a positive predictive value of 98.7%. The single-tube
assay provides confirmation of the presence of RVFV RNA for improved confidence in diagnostic
results and a "differentiate infected from vaccinated animals" (DIVA)--compatible marker for RVFV NSs
--deleted vaccines, which is useful for RVF endemic countries, but especially important in non-endemic
countries.
Impact factor: 2.065
6
MALARIA: CONTROL TO ELIMINATION (SAMJ SUPPLEMENT)
Blumberg L, D Moonasar
South Africa (SA) is one of 34 malaria-endemic countries that are currently targeting
elimination of the disease. This supplement of the SAMJ documents SA’s remarkable public
health achievement in moving from malaria control to the threshold of elimination (zero local
transmission in a defined geographical area). Nevertheless, SA’s malaria programme still needs to travel some distance
before it attains its goal of elimination by 2018. The articles in this supplement pay tribute to sterling efforts by dedicated
persons who contributed and guided policies and interventions, not only in SA, but also elsewhere on the African continent
and globally. These pioneering efforts deserve high-level recognition. The key lesson
from early malaria control is that hard-won gains are rapidly lost when important control
measures are curtailed, especially in low-transmission settings. Progress on every front,
and at every level, is fragile. Malaria is a disease that can take full advantage of any
lapse in investment, vigilance or control. SA has come a long way in fighting malaria.
This supplement is a useful reference for those keen to learn lessons from the past, and
key issues that need to be addressed to move from malaria control to elimination in SA.
These are: targeted approaches to vector control; strong programmes for detection of
parasite and vector resistance; active surveillance; ensuring that the chain of transmission is broken; regional and cross-border malaria control initiatives; and maintaining
advocacy and political commitment for the malaria programme. The benefits of elimination of the disease in SA lie in demonstrating the country’s ability to tackle a significant
public health problem, the positive impact on socioeconomic conditions and health of
persons living in affected areas, and increasing the tourism potential of the country.
Blumberg L
NICD Contributing authors to SAMJ Malaria supplement:
Frean J
Poonsamy B
Coetzee M
Mayet NT
Koekemoer L
Impact factor: 1.676
7
Brooke B
Kenyon C, Bonorchis K, Corcocan C, Meintjes G, Locketz M, Lehloenya R, Vismer HF, Naicker P, Prozesky H, van
Wyk M, Bamford C, du Plooy M, Imrie G, Dlamini S, Borman AM, Colebunders R, Yansouni CP, Mendelson M,
Govender NP. A dimorphic fungus causing disseminated infection in South Africa. The New England Journal of
Medicine. 2013 Oct 10;369(15):1416-24. doi: 10.1056/NEJMoa1215460.
Wibmer CK, Bhiman JN, Gray ES, Tumba N, Abdool Karim SS, Williamson C, Morris L, Moore PL. Viral escape
from HIV-1 neutralizing antibodies drives increased plasma neutralization breadth through sequential recognition of
multiple epitopes and immunotypes. PLoS Pathog 9(10):e1003738.doi:10.1371/journal.ppat.1003738
Wolter N, Cohen C, Tempia S, Madhi SA, Venter M, Moyes J, Walaza S, Kgokong BM, Groome M, du Plessis M,
Pretorius M, Dawood H, Kahn K, Variava E, Klugman KP, von Gottberg A. HIV and influenza infection are associated with increased blood pneumococcal load,South Africa,2009-2011. The Journal of Infectious Diseases. 2013
August: doi 10.1093/ infdis/jit427
Müller EE, Magooa MP, Lewis DA. Genetic characterization of herpes simplex virus type 2 UL23 thymidine kinase
in Johanneburg , South Africa. Journal of Antivirals & Antiretrovirals 5:080-084. doi: 10.4172/jaa.1000068
Madhi SA, Kuwanda L, Venter M, Violari A. Prospective cohort study comparing seasonal and H1N1(2009)pandemic influenza virus illnesses in HIV-infected children during 2009. The Pediatric Infectious Disease Journal.
2013 July 21; doi: 10.1097/INF 0.b013e3182a73ebb
von Gottberg A, Cohen C, de Gouveia L, Meiring S, Quan V, Whitelaw A, Crowther-Gibson P, Madhi SA, Whitney
CG, Klugman KP. Epidemiology of invasive pneumococcal disease in the pre-conjugate vaccine era: South Africa,
2003-2008.Vaccine. 2013 August 28;31(38): 4200-8 doi: 10.1016/jvaccine.2013.04.077
Venter M, van Vuren PJ, Mentoor J, Paweska J, Williams J. Vaccine. Inactivated West Nile virus (WNV) vaccine,
Duvaxyn WNV, protects against a highly neuroinvasive lineage 2 WNV strain in mice. Vaccine. 2013 Aug 20;31
(37):3856-62. doi: 10.1016/j.vaccine.2013.06.059
Alexandre K, Moore PL, Nonyane M, Gray ES, Ranchobe R, Chakauya E, McMahon J, O’Keefe B, Chikwamba R,
Morris L. Mechanisms of HIV-1 subtypes resistance to GRFT,CV-N and SVN. Virology. 2013 Nov;446(1-2):66-76.
doi: 10.1016/j.virol.2013.07.019
Lewis DA, Marsh K, Radebe F, Maseko V, Hughes G. Trends and associations of Trichomonas vaginalis infection
in men and women with genital discharge syndromes in Johannesburg, South Africa. Sexually Transmitted
Infections. 2013 Sep;89(6):523-7. doi: 10.1136/sextrans-2013-051049
Mogoye BK, Menezes CN, Wong ML, Stacey S, von Delft D, Wahlers K, Wassermann M, Romig T, Kern P, Grobusch
MP, Frean J . First Insights into species and genotypes of Echinococcus in South Africa. Veterinary Parasitology.2013.
Sep 23;196(3-4):427-32. doi: 10.1016/j.vetpar.2013.03.033.
Wilson WC, Romito M, Jasperson DC, Weingartl H, Binepal YS, Maluleke MR, Wallace DB, van Vuren PJ, Paweska JT.
Developments of Rift Valley fever real time PCR-assay that can detect all three genome segments. Journal of Virological
Methods. 2013 Nov;193(2):426-31. doi: 10.1016/j.jviromet.2013.07.006.
Blumberg L, Moonasar D. Malaria: control to elimination. South African Medical Journal 2013;103(10):769.
doi:10.7196/samj.7401
This issue of Science Focus includes publications in the report covering the period July 2013 – September 2013.
The abstracts are extracted directly from the publications.
Published by NICD Communications. For comments and queries please email: nombusos@nicd.ac.za
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