Joseph DeRisi

Last updated
Joseph DeRisi
Joseph DeRisi 2021.jpg
Nationality American
Alma mater Stanford University, University of California, Santa Cruz
Known forViroChip, work on identifying SARS virus, gene expression in Plasmodium falciparum
Scientific career
Fields Biology
Institutions University of California, San Francisco Howard Hughes Medical Institute
Thesis The Analysis of whole genome gene expression in the budding yeast Saccharomyces cerevisiae.  (1999)
Doctoral advisor Patrick O. Brown

Joseph Lyman DeRisi is an American biochemist, specializing in molecular biology, parasitology, genomics, virology, and computational biology.

Contents

Early life and education

DeRisi was raised in Carmichael, California, where he graduated from Del Campo High School. [1] He received a B.A. in Biochemistry and Molecular Biology in 1992 from the University of California, Santa Cruz. [2]

DeRisi earned his Ph.D. in biochemistry from Stanford University in 1999. Working in the laboratory of Patrick O. Brown, he developed methods for the production and use of DNA microarrays in molecular biology, and his thesis was a genome-wide expression analysis of the budding yeast S. cerevisiae. [3] [4] [5] Upon graduation, DeRisi accepted a position as a Sandler Fellow at the University of California San Francisco. [2] [6]

Career and research

DeRisi has been a faculty member of the UCSF biochemistry and biophysics department since 1999. As of 2022 he is a professor of biochemistry and biophysics and is also the director of UCSF's Sandler Program for Breakthrough Biomedical Research. [2] [6]

DeRisi is known for printing the first whole-genome expression array, [7] performing the first broad analysis of differential gene expression in cancer cells, [8] profiling gene expression throughout the lifecycle of the malaria-causing protozoan Plasmodium falciparum , [9] genomic characterization of the SARS-CoV-1 virus, [10] and pioneering virus discovery using gene hybridization arrays and DNA sequencing technologies. [11]

In his early career, DeRisi was a pioneer of microarrays, and designed and built both hardware and software for microarrays. He was a proponent of open access to microarray technology, [5] and maintained a website with software and protocols for microarray operations. [4] He is also a proponent of open access publishing. [12]

In 2002, DeRisi and his research collaborator David Wang developed the ViroChip, a DNA microarray that could be used to rapidly identify viruses in a sample of blood or tissue. [13] He used the tool to help identify the SARS-CoV-1 virus in 2003. In 2004, DeRisi was named a MacArthur fellow (the "Genius" award) for his work with ViroChip and genomic diagnostic techniques. [12] [14]

DeRisi became a Howard Hughes Medical Institute (HHMI) investigator in 2005, and received financial support from HHMI for his research. [6] [15] He remained an investigator until 2016. [16]

DeRisi and his colleagues employ metagenomic next-generation sequencing (mNGS) for applications including to identify the causal agents in cases of infectious encephalitis and meningitis and to discriminate between autoimmune and infectious causes, diagnosing cases that are difficult to decipher using traditional clinical laboratory techniques. [13] [17] Using metagenomic sequencing, DeRisi has identified disease-causing viruses in humans, and in animals ranging from parrots and cockatiels to honeybees and boa constrictors. [13] [18] He and a research partner, Don Ganem, have identified a parasite, Nosema ceranae , that appears to be responsible for colony collapse among honeybees. [19] He has also de-bunked the relation of viruses to certain subsets of human cancer. [20]

DeRisi and his colleague Dr. Michael Wilson used a phage display to screen antibody samples from patients with autoimmune symptoms against a library of human proteins, allowing them to identify a cancer-associated autoantigen that is the cause of the symptoms. [20] [21]

DeRisi’s lab at UCSF also conducts research to understand the genetics of the malaria-causing pathogen Plasmodium falciparum , the causative agent of the most deadly form of human malaria. [12] [22] DeRisi's group has developed candidate drugs to cure malaria. [23] In 2011, the group determined the function of the apicoplast, a unique organelle in apicomplexans, identifying the target of an anti-malarial drug that was a preclinical candidate. [24] [25]

In 2016, DeRisi became the co-president of the newly established CZ Biohub, alongside Stephen Quake. [26] After joining CZ Biohub, DeRisi established a team of developers to create a cloud-based metagenomic diagnostic platform based on code from his lab at UCSF. The platform, then named IDSeq, was initially launched for testing by a small group in 2018. [27] [17] The development and computing costs were backed by the Chan Zuckerberg Initiative and CZ Biohub. [17] The platform is used to rapidly identify pathogens from metagenomic sequencing data, [28] and as of 2022 is known as CZ-ID. [29]

In 2020, early in the COVID-19 pandemic, DeRisi led a team that turned an empty lab space adjacent to the CZ Biohub into a CLIA-certified COVID-19 testing facility in eight days. [30] [31] CLIAhub became one of the nation's leading COVID-19 testing centers, processing thousands of tests per day and becoming a model for the nation. [32] [33] [34] DeRisi’s early warning of the pandemic and development of rapid testing technology was documented by Michael Lewis in his book The Premonition: A Pandemic Story. [35] [36] At the same time, DeRisi became an active proponent of developing a national COVID-19 surveillance system to identify and monitor mutations in the COVID-19 virus. [37] [38] [33]

Awards and honors

And Membership in scientific organizations would contain:

Related Research Articles

<span class="mw-page-title-main">Malaria</span> Mosquito-borne infectious disease

Malaria is a mosquito-borne infectious disease that affects humans and other vertebrates. Human malaria causes symptoms that typically include fever, fatigue, vomiting, and headaches. In severe cases, it can cause jaundice, seizures, coma, or death. Symptoms usually begin 10 to 15 days after being bitten by an infected Anopheles mosquito. If not properly treated, people may have recurrences of the disease months later. In those who have recently survived an infection, reinfection usually causes milder symptoms. This partial resistance disappears over months to years if the person has no continuing exposure to malaria.

<i>Plasmodium falciparum</i> Protozoan species of malaria parasite

Plasmodium falciparum is a unicellular protozoan parasite of humans, and the deadliest species of Plasmodium that causes malaria in humans. The parasite is transmitted through the bite of a female Anopheles mosquito and causes the disease's most dangerous form, falciparum malaria. It is responsible for around 50% of all malaria cases. P. falciparum is therefore regarded as the deadliest parasite in humans. It is also associated with the development of blood cancer and is classified as a Group 2A (probable) carcinogen.

<span class="mw-page-title-main">Fosmidomycin</span> Chemical compound

Fosmidomycin is an antibiotic that was originally isolated from culture broths of bacteria of the genus Streptomyces. It specifically inhibits DXP reductoisomerase, a key enzyme in the non-mevalonate pathway of isoprenoid biosynthesis. It is a structural analogue of 2-C-methyl-D-erythrose 4-phosphate. It inhibits the E. coli enzyme with a KI value of 38 nM (4), MTB at 80 nM, and the Francisella enzyme at 99 nM. Several mutations in the E. coli DXP reductoisomerase were found to confer resistance to fosmidomycin.

<i>Plasmodium berghei</i> Single celled parasite, rodent malaria

Plasmodium berghei is a single-celled parasite causing rodent malaria. It is in the Plasmodium subgenus Vinckeia.

An apicoplast is a derived non-photosynthetic plastid found in most Apicomplexa, including Toxoplasma gondii, and Plasmodium falciparum and other Plasmodium spp., but not in others such as Cryptosporidium. It originated from algae through secondary endosymbiosis; there is debate as to whether this was a green or red alga. The apicoplast is surrounded by four membranes within the outermost part of the endomembrane system. The apicoplast hosts important metabolic pathways like fatty acid synthesis, isoprenoid precursor synthesis and parts of the heme biosynthetic pathway.

Malaria vaccines are vaccines that prevent malaria, a mosquito-borne infectious disease which annually affects an estimated 247 million people worldwide and causes 619,000 deaths. The first approved vaccine for malaria is RTS,S, known by the brand name Mosquirix. As of April 2023, the vaccine has been given to 1.5 million children living in areas with moderate-to-high malaria transmission. It requires at least three doses in infants by age 2, and a fourth dose extends the protection for another 1–2 years. The vaccine reduces hospital admissions from severe malaria by around 30%.

PfATP6, also known as PfSERCA or PfATPase6, is a calcium ATPase gene encoded by the malaria parasite Plasmodium falciparum. The protein is thought to be a P-type ATPase involved in calcium ion transport.

Pregnancy-associated malaria (PAM) or placental malaria is a presentation of the common illness that is particularly life-threatening to both mother and developing fetus. PAM is caused primarily by infection with Plasmodium falciparum, the most dangerous of the four species of malaria-causing parasites that infect humans. During pregnancy, a woman faces a much higher risk of contracting malaria and of associated complications. Prevention and treatment of malaria are essential components of prenatal care in areas where the parasite is endemic – tropical and subtropical geographic areas. Placental malaria has also been demonstrated to occur in animal models, including in rodent and non-human primate models.

<span class="mw-page-title-main">RTS,S</span> Malaria vaccine

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Plasmodium falciparum erythrocyte membrane protein 1 (PfEMP1) is a family of proteins present on the membrane surface of red blood cells that are infected by the malarial parasite Plasmodium falciparum. PfEMP1 is synthesized during the parasite's blood stage inside the RBC, during which the clinical symptoms of falciparum malaria are manifested. Acting as both an antigen and adhesion protein, it is thought to play a key role in the high level of virulence associated with P. falciparum. It was discovered in 1984 when it was reported that infected RBCs had unusually large-sized cell membrane proteins, and these proteins had antibody-binding (antigenic) properties. An elusive protein, its chemical structure and molecular properties were revealed only after a decade, in 1995. It is now established that there is not one but a large family of PfEMP1 proteins, genetically regulated (encoded) by a group of about 60 genes called var. Each P. falciparum is able to switch on and off specific var genes to produce a functionally different protein, thereby evading the host's immune system. RBCs carrying PfEMP1 on their surface stick to endothelial cells, which facilitates further binding with uninfected RBCs, ultimately helping the parasite to both spread to other RBCs as well as bringing about the fatal symptoms of P. falciparum malaria.

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