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Williams, B. G.

Publications and source records attributed to Williams, B. G..

12 recordsLinked to original sources

De novo minibinders targeting RH5 achieve nanomolar inhibition of blood-stage malaria replication

Malaria kills {approx}600,000 people annually despite recently deployed vaccines. The parasite's blood-stage invasion of erythrocytes, driven by the essential, non-redundant interaction between Plasmodium falciparum RH5 and erythrocyte basigin, remains a leading therapeutic target. Here, we designed de novo mini-proteins (minibinders) to occlude this interface. From {approx}1,500 computationally generated designs, we synthesized 18 candidates ranging from 9.3 to 16.9 kDa which were easily expressed in E. coli as soluble, well-folded proteins. Of these, 7 minibinders blocked blood-stage replication of P. falciparum asexual stage parasites with greater potency than {approx}300nM IC50. Three potent candidate minibinders, mb-5, mb-7, and mb-21, were confirmed to bind RH5 via SPR and BLI and block the merozoite-to-ring transition in stage-synchronized parasite progression assays, with CryoEM of minibinder-RH5 complex confirming the predicted binding at RH5-basigin interface. Although pharmacological challenges remain, our data demonstrate that potent inhibitors of parasite growth, rivaling existing antimalarials, can be designed rather than discovered via extensive screening. Our data highlight the potential for artificial intelligence to change the development landscape of new antimalarial therapies.

microbiology↗

Structural basis for synergistic antibody protection against the essential malaria invasion complex protein RIPR

Plasmodium falciparum RH5-interacting protein (RIPR) is central to the essential PTRAMP-CSS-RIPR-CyRPA-RH5 (PCRCR)-complex; a leading target of blood-stage malaria vaccines. However, mechanisms whereby anti-RIPR antibodies inhibit parasite invasion are poorly understood. Here, we characterise 83 human IgG mAbs from RIPR-vaccinated Kymouse platform mice. Single mAbs have minimal neutralising activity, however, high-level synergistic inhibition is observed with pools of mAbs targeting the RIPR-Tail region. Structural characterisation and molecular dynamics simulations of RIPR-Tail show that mAbs targeting EGF-like domains 6-8 (RIPREGF (6-8)), but not EGF-like domains 9-10 or the C-terminal domain (RIPREGF (9-10)-CTD), synergise to constrain the RIPR-Tail conformation. The same antibodies dissociate PTRAMP-CSS from RIPR, thereby enabling anti-RIPREGF (9-10)-CTD mAbs or anti-CSS sdAbs to bind and potentiate anti-RIPREGF (6-8) IgG. Addition of these mAbs to IgG from humans immunised with the R78C (RIPREGF (7-8)-CyRPA) candidate vaccine enhances malaria growth inhibition. These data provide a framework to guide next-generation blood-stage malaria vaccine design.

immunology↗

Evaluating the potential of cross-species neutralization of anti-PfCyRPA and anti-PfRIPR Monoclonal Antibodies

PfCyRPA and PfRIPR are promising next-generation malaria blood-stage vaccine candidate antigens that play an essential role in erythrocyte invasion of Plasmodium falciparum. CyRPA and RIPR orthologs are present in all human-infecting Plasmodium species, suggesting the potential for a cross-species vaccine. Using Growth Inhibition Assays (GIA), this study investigates seven anti-PfCyRPA and three anti-PfRIPR monoclonal antibodies targeting P. falciparum for their inhibitory activity against P. knowlesi, a non-falciparum species that contributes to a significant burden of zoonotic disease in South-East Asia, shares some biological features with Plasmodium vivax, and has a robust in vitro culture system. Despite their efficacy against P. falciparum and partially conserved epitopes, these antibodies exhibited minimal inhibition of P. knowlesi. Understanding the antigenic diversity and immune mechanisms across Plasmodium species is critical for advancing pan-species vaccine strategies.

immunology↗

Development of an improved blood-stage malaria vaccine targeting the essential RH5-CyRPA-RIPR invasion complex

In recent years, reticulocyte-binding protein homologue 5 (RH5) has emerged as a leading blood-stage Plasmodium falciparum malaria vaccine antigen. The most advanced blood-stage vaccine candidate in a Phase 2b clinical trial, RH5.1/Matrix-M, is based on a full-length soluble protein-with-adjuvant formulation. RH5 interacts with cysteine-rich protective antigen (CyRPA) and RH5- interacting protein (RIPR) to form an essential heterotrimeric "RCR-complex". Here, we investigated whether a vaccine candidate based on the ternary RCR-complex could substantially improve upon the leading clinical candidate RH5.1/Matrix-M in preclinical studies. Using a panel of monoclonal antibodies (mAbs) we confirm that parasite growth-inhibitory epitopes on each antigen are exposed on the surface of the RCR-complex and that mAb pairs binding to different antigens can function additively or synergistically to mediate parasite growth inhibition activity (GIA) in vitro. However, immunisation of rats with the RCR-complex consistently fails to outperform RH5.1 alone. We show this is due to immuno-dominance of RIPR coupled with the inferior potency of anti-full length RIPR polyclonal IgG antibodies as compared to the anti-RH5 and anti-CyRPA response. To address this, we identified the growth-inhibitory antibody epitopes of RIPR are clustered within C-terminal EGF-like domains of RIPR. A fusion of these EGF domains to CyRPA, called "R78C", combined with RH5.1, provided a new vaccination strategy that improves upon the levels of in vitro GIA seen with RH5.1 alone. Superiority of the combination antigen vaccine candidate was achieved by the induction of a quantitatively higher, but qualitatively similar, polyclonal antibody response that demonstrated additive GIA across the three antigen targets. These preclinical data justified the advancement of the RH5.1+R78C/Matrix-M combination vaccine to a Phase 1 clinical trial.

immunology↗

Preclinical Development of a Stabilized RH5 Virus-Like Particle Vaccine that Induces Improved Anti-Malarial Antibodies

The development of a highly effective vaccine against the pathogenic blood-stage infection of human malaria will require a delivery platform that can induce an antibody response of both maximal quantity and functional quality. One strategy to achieve this includes presenting antigens to the immune system on virus-like particles (VLPs). Here we sought to improve the design and delivery of the blood-stage Plasmodium falciparum reticulocyte-binding protein homolog 5 (RH5) antigen, which is currently in a Phase 2 clinical trial as a full-length soluble protein-in-adjuvant vaccine candidate called RH5.1/Matrix-M. We identify disordered regions of the full-length RH5 molecule induce non-growth inhibitory antibodies in human vaccinees, and a re-engineered and stabilized immunogen that includes just the alpha-helical core of RH5 induces a qualitatively superior growth-inhibitory antibody response in rats vaccinated with this protein formulated in Matrix-M adjuvant. In parallel, bioconjugation of this new immunogen, termed "RH5.2", to hepatitis B surface antigen VLPs using the "plug-and-display" SpyTag-SpyCatcher platform technology also enabled superior quantitative antibody immunogenicity over soluble antigen/adjuvant in vaccinated mice and rats. These studies identify a new blood-stage malaria vaccine candidate that may improve upon the current leading soluble protein vaccine candidate RH5.1/Matrix-M. The RH5.2-VLP/Matrix-M vaccine candidate is now under evaluation in Phase 1a/b clinical trials.

immunology↗

Analysis of the Diverse Antigenic Landscape of the Malaria Invasion Protein RH5 Identifies a Potent Vaccine-Induced Human Public Antibody Clonotype

The highly conserved and essential Plasmodium falciparum reticulocyte-binding protein homolog 5 (PfRH5) has emerged as the leading target for vaccines that seek to protect against the disease-causing blood-stage of malaria. However, the features of the human vaccine-induced antibody response that confer highly potent inhibition of malaria parasite invasion into red blood cells are not well defined. Here we characterize over 200 human IgG monoclonal antibodies induced by the most advanced PfRH5 vaccine. We define the antigenic landscape of this molecule, and establish epitope specificity, antibody association rate and intra-PfRH5 antibody interactions are key determinants of functional anti-parasitic potency. In addition, we identify a germline gene combination that results in an exceptionally potent class of antibody and demonstrate its prophylactic potential to protect against P. falciparum parasite challenge in vivo. This comprehensive dataset provides a framework to guide rational design of next-generation vaccines and prophylactic antibodies to protect against blood-stage malaria.

immunology↗

The Dual Action of Human Antibodies Specific to Plasmodium falciparum PfRH5 and PfCyRPA: Blocking Invasion and Inactivating Extracellular Merozoites

The Plasmodium falciparum reticulocyte-binding protein homolog 5 (PfRH5) is the current leading blood-stage malaria vaccine candidate. PfRH5 functions as part of the pentameric PCRCR complex containing PTRAMP, CSS, PfCyRPA and PfRIPR, all of which are essential for infection of human red blood cells (RBCs). To trigger RBC invasion, PfRH5 engages with RBC protein basigin in a step termed the RH5-basigin binding stage. Although we know increasingly more about how antibodies specific for PfRH5 can block invasion, much less is known about how antibodies recognizing other members of the PCRCR complex can inhibit invasion. To address this, we performed live cell imaging using monoclonal antibodies (mAbs) which bind PfRH5 and PfCyRPA. We measured the degree and timing of the invasion inhibition, the stage at which it occurred, as well as subsequent events. We show that parasite invasion is blocked by individual mAbs, and the degree of inhibition is enhanced when combining a mAb specific for PfRH5 with one binding PfCyRPA. In addition to directly establishing the invasion-blocking capacity of the mAbs, we identified a secondary action of certain mAbs on extracellular parasites that had not yet invaded where the mAbs appeared to inactivate the parasites by triggering a developmental pathway normally only seen after successful invasion. These findings suggest that epitopes within the PfCyRPA-PfRH5 sub-complex that elicit these dual responses may be more effective immunogens than neighboring epitopes by both blocking parasites from invading and rapidly inactivating extracellular parasites. These two protective mechanisms, prevention of invasion and inactivation of uninvaded parasites, resulting from antibody to a single epitope indicate a possible route to the development of more effective vaccines. Author SummaryMalaria is a sometimes-fatal disease caused by protozoan parasites of which Plasmodium falciparum is the most deadly species that causes hundreds of millions of infections and half a million deaths per year. A partially effective vaccine is available to block parasite forms transmitted by mosquitoes but not the subsequent blood stage which causes symptomatic disease. To fight blood stage parasites, proteins have been identified such as PfRH5, that aid parasite entry into human red blood cells (RBCs) and vaccines made from these proteins can trigger the production of antibodies that bind the parasite proteins thereby blocking RBC invasion. PfRH5 forms a complex with another parasite protein called PfCyRPA and together antibodies to PfCyRPA and PfRH5 are highly effective in reducing parasite growth. Here we investigated how antibodies to PfCyRPA and PfRH5 actually block invasion using video microscopy of live parasites. As anticipated, we found the antibodies not only stopped most parasites from invading but of those parasites that did invade, they took longer to do so, suggesting the antibodies were physically inhibiting the invasion process. One unanticipated effect of both PfRH5 antibodies and one of three PfCyRPA antibodies tested, was that they triggered the uninvaded parasites to change into cellular forms normally only seen inside RBCs. These intracellular forms are no longer competent to invade and so the PfRH5/CyRPA antibodies have the potential of both neutralize parasites by physically preventing RBC entry and by changing the parasites into invasion incompetent forms.

microbiology↗

Antiretroviral therapy is the principal cause of tuberculosis decline in southern and eastern Africa

The incidence of tuberculosis (TB) in southern and eastern Africa was driven sharply upwards during 1980s and 1990s by coinfection with Mycobacterium tuberculosis and the human immunodeficiency virus (HIV). Although drug treatments for TB infection (isoniazid preventive therapy) and disease (combinations of TB drugs) can reduce TB incidence if implemented effectively, we find that antiretroviral therapy (ART) given to people with HIV infection was strongly and systematically associated with the accelerated decline of TB in 12 of the worst affected African countries between 2003 and 2016. Inferring that ART was a significant cause of TB decline, ART prevented approximately 1.88 {+/-} 0.23 million HIV-positive TB cases, or 15.7 {+/-} 1.9 percent of the total number expected. There is no evidence that drug treatment of TB infection (IPT) or disease (combination chemotherapy) played more than a minor role in accelerating TB decline after 2003. In these 12 countries, over the period 2003-16, ART made a major contribution towards achieving international targets for the reduction of TB incidence.\n\nSignificanceTuberculosis (TB) is still the leading cause of death from a single infectious agent. To cut the TB incidence rate by 80% between 2015 and 2030, in line with the WHO End TB Strategy, demands a five-fold increase in the rate of decline worldwide, from 2% to 10%/year. We find that the reduction in TB incidence rate in 12 African countries, at up to 8%/year, is due mainly to the expanded provision of antiretroviral therapy (ART) to people living with HIV, rather than to improvements in the treatment of TB infection and disease. ART should remain central to TB control where rates of TB-HIV coinfection are high, but new efforts are needed to maximize the direct benefits of treating TB infection and disease.

epidemiology↗

HIV-Attributed Causes of Death in the Medical Ward at the Chris Hani Baragwanath Hospital, South Africa

BackgroundThere are sparse data in Africa on the association between HIV infection and deaths from underlying medical conditions. Using records from the Chris Hani Baragwanath Hospital (CHBH) in Soweto, South Africa, we determined mortality from medical conditions associated with HIV.\n\nMethodsFrom January 2006 to December 2009 AB collected data on 15,725 deaths including age, sex, day of admittance and death, HIV status, ART initiation and CD4+ cell counts and reviewed the underlying cause of death using medical notes. Conditions known to be associated with HIV were cases; conditions not associated with HIV were controls. We calculate the HIV odds-ratios for cases relative to controls and HIV-attributable deaths as the fraction of those with each condition, the disease-attributable fraction (DA), and as the fraction of all deaths, the population-attributable fraction (PAF).\n\nInterpretationThe high prevalence of HIV among those that died in the medical wards at the CHBH, especially in those below the age of 50 years, demonstrates the impact of the HIV-epidemic on adult mortality and hospital services and the extent to which early antiretroviral treatment would have reduced the burden of both. Of the deaths included in the analysis the prevalence of HIV was 61% and the prevalence of AIDS related conditions was 69%. The HIV-attributable fraction was 36% in the whole sample and 60% in those that were HIV-positive. Cryptococcosis, Kaposis sarcoma and Pneumocystis jeroveci are highly predictive of HIV while TB, gastroenteritis and anaemia are very strongly associated with HIV. The greatest number of deaths attributable to HIV was among those dying of TB or of other respiratory conditions.\n\nFundingNo funding was received for this study.

epidemiology↗

Ending AIDS: trends in the incidence of HIV in eastern and southern Africa

While great progress has been made in the control and management of the HIV epidemic there is still much to be done. Using trends in the rate of new HIV infections in eastern and southern Africa we assess the current state of the epidemic and evaluate the future prospects for controlling it. If we let an incidence of 1 per 1,000 people represent a control threshold then this has been reached, or will probably be reached by 2020, in eastern Africa and is reachable by 2020 in those southern African countries that do not have particularly strong social and economic ties to South Africa if they continue to scale up their treatment programmes. In South Africa and its immediate neighbours Lesotho, Mozambique and Swaziland, the prospects are less certain. These countries are unlikely to reach the control threshold by 2020 but with sufficient political will and commitment to treatment for all could do so by 2030.\n\nThere are two important caveats. First, reaching the control threshold still leaves 35 thousand new infections a year. As the lessons of polio remind us, finding the last few, hard to reach cases will demand more focussed strategies. Second, ending AIDS will not end HIV and about 35 million people will have to be kept on ART for the next 30 to 40 years unless and until a cure is discovered. Even if we assume a modest cost of, say, US$100 per person per year for ART treatment and support, this corresponds to a continuing financial commitment of US$3.5 Bn per year although this is substantially less than the approximately US$ 40 Bn per year currently committed to HIV and AIDS.

epidemiology↗

Dynamics and Control of Infections on Social Networks of Population Types

Random mixing in host populations has been a convenient simplifying assumption in the study of epidemics, but neglects important differences in contact rates within and between population groups. For HIV/AIDS, the assumption of random mixing is inappropriate for epidemics that are concentrated in groups of people at high risk, including female sex workers (FSW) and their male clients (MCF), injecting drug users (IDU) and men who have sex with men (MSM). To find out who transmits infection to whom and how that affects the spread and containment of infection remains a major empirical challenge in the epidemiology of HIV/AIDS. Here we develop a technique, based on the routine sampling of infection in linked population groups (a social network of population types), which shows how an HIV/AIDS epidemic in Can Tho Province of Vietnam began in FSW, was propagated mainly by IDU, and ultimately generated most cases among the female partners of MCF (FPM). Calculation of the case reproduction numbers within and between groups, and for the whole network, provides insights into control that cannot be deduced simply from observations on the prevalence of infection. Specifically, the per capita rate of HIV transmission was highest from FSW to MCF, and most HIV infections occurred in FPM, but the number of infections in the whole network is best reduced by interrupting transmission to and from IDU. This analysis can be used to guide HIV/AIDS interventions using needle and syringe exchange, condom distribution and antiretroviral therapy. The method requires only routine data and could be applied to infections in other populations.

epidemiology↗

90-90-90, epidemic control, and ending AIDS: review of global situation and recommendations

HIV remains a devastating pandemic HIV remains a devastating... Ending AIDS The prevention vs. treatment... Economics of ending AIDS Major innovations accelerating... HIV self-tests Universal treatment regimen Comprehensive community-based... Standardized M and E... Unification of global leadership... Last mile strategies,... Conclusion References Although human immunodeficiency virus (HIV) first came to our attention thirty-seven years ago, the acquired immunodeficiency syndrome (AIDS) which it causes is, without treatment, 100% fatal with devastating consequences for millions of people1. More than 35 million people have already died of ...

epidemiology↗