If a patient stays on a regimen until only latent cells are left, we can then use a latent-specific immune cell activator to purge these last remaining infected cells. However, the latter part of this treatment methodology has yet to be discovered; until it is, yes the patient must remain on the drugs for as long as possible.
The drugs in the cocktail would not create selective pressure for alternate receptors since they all act on aspects of the virus life cycle downstream of the receptor/entry point.
The HIV virus does not "embed" itself into the dna of a victim. Lesson on the viral life cycle:
HIV --> injects RNA genome + tRNA primer --> reverse transcription to double stranded DNA --> integration ("embedding") into host genome --> transcription of viral genes from integrated HIV DNA to spliced and unspliced mRNA--> translation/export of mRNA and formation of virus particles
It inserts it's rna into t-cells and uses the t-cells to replicate itself. The problem is that this kills the t-cells, thus killing you. The cause of massive T cell loss in HIV infection has yet to be concretely determined. Direct cell killing due to viral cytopathic effect is not believed to be a major factor. Rather the dysregulation of immune activation, function and apoptosis associated with infection are thought to be the primary causes for T cell loss. Your death is also not a direct effect of T cell loss, but rather the emergence of a combination of opportunistic infections and oncogenic viruses such as Kaposi's Sarcoma Herpesvirus which kills a person.
It does NOT hide away and wait to pop out the second a victim stops taking his or her cocktail.
And actually, the latent reservoir DOES wait to pop out the second a victim stops taking his/her cocktail. It isn't quite as malicious as you imply though...the "popping out" occurs naturally as cells from the resting memory reservoir are activated by antigen stimulus and then reinitiate productive infection. This occurs periodically even when a patient is on medications, but fail to produce virus due to drug blocking virus life cycle. But when a patient has to inevitably stop treatment due to prohibitive cost, toxicity or other side effects, these re-activation events are allowed to proceed and reinitiate full-blown infection.
It cannot attack neurons. Only t-cells.
It has been shown that HIV can enter neurons, but it just fails to produce virus. HIV infects not only T cells, but macrophages as well. Additionally, some groups have reported evolution of viruses which can use their co-receptors as the entry point, opening HIV to a wider range of host cells.
Sorry about this double post, low sleep = mistakes. But I wanted the full and proper reply to go up.
Using highly active anti-retroviral treatment (HAART) regimens comprised of a combination of 3-4 drugs from the following classes: protease inhibitors, non-nucleoside reverse transcriptase inhibitors, nucleoside reverse transcriptase inhibitors, we can essentially eliminate all productively infected cells and the only infected cells remaining are transcriptionally latent, producing no new virus, causing no symptoms and giving the patient essentially virus-free blood. There are a number of suspected "reservoir" populations where latently infected cells can be found (resting memory CD4 T cells, macrophages). Only latently infected memory T cells have been proven to be clinically relevant. The stats on infection for these cells are that on average around 1 in every 10^6 resting memory CD4 T cells is latently infected in any given patient. This number can vary between HAART patients from less than 1 in 10^6 to even 10s in 10^6. In order for HIV to replicate, it must integrate itself into the host cell's DNA in every infected cell. Only a select few cells will integrate, then become latent and enter hibernation. Eliminating these cells will not likely cause any perceptible deficit in immune function.
HIV infects cells of the immune system; HIV's receptor is CD4, coreceptors are CXCR4 and CCR5, all found exclusively on immune cells, not neurons. The cell death and dementia associated with HIV is most likely a bystander effect, where immune cells in the brain are replicating virus and some product or downstream effect of the replication cycle is causing neighboring cells to die. Again though, the number of infected cells is low. The main issue with the brain is that it is immune privileged, so it is under less rigorous immune surveillance than the rest of the body. Combine that fact with the fact that HIV infects immune cells and disrupts their function, and you have a recipe for disaster in the brain. Antiretrovirals that can penetrate the BBB can effectively stop virus replication there without destroying nervous function.
Using highly active anti-retroviral treatment (HAART) regimens comprised of a combination of 3-4 drugs from the following classes: protease inhibitors, non-nucleoside reverse transcriptase inhibitors, nucleoside reverse transcriptase inhibitors, we can essentially eliminate all productively infected cells and the only infected cells remaining are transcriptionally latent, producing no new virus, causing no symptoms and giving the patient essentially virus-free blood. There are a number of suspected "reservoir" populations where latently infected cells can be found (resting memory CD4 T cells, macrophages). Only latently infected memory T cells have been proven to be clinically relevant. The stats on infection for these cells are that on average around 1 in every 10^6 resting memory CD4 T cells is latently infected in any given patient. This number can vary between HAART patients to
HIV infects cells of the immune system; HIV's receptor is CD4, coreceptors are CXCR4 and CCR5, all found exclusively on immune cells, not neurons. The cell death and dementia associated with HIV is most likely a bystander effect, where immune cells in the brain are replicating virus and some product or downstream effect of the replication cycle is causing neighboring cells to die. Again though, the number of infected cells is low. The main issue with the brain is that it is immune privileged, so it is under less rigorous immune surveillance than the rest of the body. Combine that fact with the fact that HIV infects immune cells and disrupts their function, and you have a recipe for disaster in the brain. Antiretrovirals that can penetrate the BBB can effectively stop virus replication there without destroying nervous function.
Never say never. I think there are a number of studies that have yet to be done on latently infected cells with integrated HIV. Without fully characterizing the latent cells, we can't really say that there isn't something different about them that can't be exploited for targeting treatments.
If leaders of the field are to be believed, anti-retroviral drug regimens can currently eliminate all infected cells in the body save for these latently infected ones. And if developments arise that allow specific targeting and elimination of the latent cells, boom problem is solved. I'm prophesizing a system of targeted immune activation to draw out the hiding infected cells, and letting existing drugs get rid of em.
I think the problem of replication and infection in the brain is also poorly understood. Personally, I think the extravasation of infected immune cells into the brain is the source of replication, rather than any of the resident cells. The cells in the brain that can host replication are extremely limited (microglia, barely in astrocytes), and there are already promising developments to stop replication with drugs that easily cross the blood brain barrier (minocycline stops hiv replication in microglia, attenuates neuronal apoptosis).
Gene therapy to deliver RNAi targeting HIV mRNAs offers another potential solution to this whole problem. I think the tools and most of the knowledge are out there. We just need to develop them to the point of usability. However, I really have little faith in the utility of the drug outlined in this study. Tons of crap kills HIV in a test tube. Let's see how toxic this drug is and its bioavailability/pharmocokinetic profile.
I see a huge loophole in this thinking. Free radicals and reactive oxygen species, while bad in excess, are involved in numerous signaling pathways of the body and are enormously important in phenomena like immune activation. Massive supplementing of anti-oxidants may address the suspected negative role of oxidative stress in shortening telomeres , but raises tons of others. If you dose yourself with anti-oxidants and screw up the normal thresholds for oxidant-related signaling, who knows what myriad of negative effects may arise?
Jeez o flip people, read the blasted article. They want to identify pathways involved in pressure sensing, not just to determine cause of death. This has implications in general biology and is hardly mindless killing of rodents. Now I'm not saying that this couldn't have been done without sacrifice of the animal, but I would imagine it would be quite hard to get a good mRNA profile of a cell under transient mechnical pressure. Really, how the hell would you do that?
As for all you broadly anti-animal testing people...I can only say that as an SIV monkey researcher myself, really the best and only truly valuable way to study pathophysiology of mant diseases is with an animal model. Really anything in cell culture is much less useful considering how things change when you scale up into an animal with multiple organ systems. Sad but true. So some monkeys/mice/dogs/cats/guinea pigs/ferrets/flies/sea urchins/etc gotta go. I really want to see more sea urchins on PETA shirts though. That would make my day.
Reading the article, they actually attribute the difference in expression less to lack of oxygen and more to mechanosensing of compression of the skin. This is what I was thinking as I was reading the news summary.
The results may contribute to clarifying the pathophysiology of compression of the skin and may be useful in the diagnosis of suffocation.
Either way you look at it, this kind of activity is pretty obvious to occur when when you consider all the stress and environment sensing signaling pathways that a cell has (heat, pressure, mechanical forces, gas and liquid ion concentrations etc).
My one major grip is that in the article they really needed to better control the position of the cells analyzed to the site of insult. What would've been cool is if they had seen a graident effect of gene expression, highest in cells near d=0 (site of strangulation/string contact) and tapering as you examined cells farther away in the neck. This would also provide more evidence on the theory of mechanosensing since as you move away from d=0, the mechanical force on the cells decreases. The 4 genes found upregulated only really has one solid link to the cytoskeleton and gives evidence of a compression-sensitive signaling pathway.
The sequence of S1 precisely agreed with FGD1 mRNA, which is a member of the diffuse B-cell lymphoma (DBL) homology family proteins [5]...FGD1 acts only upon Cdc42, which is a member of the Rho family and has many functions such as regulating the actin cytoskeleton and intracellular adhesion [6].
Ikematsu I., et al. Legal Medicine article in press, (2006)
the reason there is usage for tons of blood problems is that the primary type of progenitor cell in cord blood is in fact hematopoietic stem cells (blood cell progenitors); the potential differentiation fates of these cells are not fully fleshed out, so we are just kind of guessing that these stem cells can form any cell in the blood. there is the possibility that in cord blood, there may be mesenchymal and neural precursors (hence interest in neurodegenerative and muscoloskeletal disease), but really we don't know what stem cells are in cord blood and showing potential to differentiate into neural, endothelial and other mesenchymally derived cells.
i think priority needs to go into embryonic, toti-potent cells so that we can understand the process of differentiation completely, and then we will know exactly where we stand with the potential cell fates of other types of stem cells we have less controversial access to (cord blood stem cells, adult bone marrow etc) and can actually make them therapeutically viable with cell culture methods ex vivo.
starting major therapeutic research with hematopoietic stem cells seems alot to me like starting to build a building by stacking premade floors instead of hiring an architect and engineer.
The most common human cell-based therapy applied today is hematopoietic stem cell (HSC) transplantation. Currently, human bone marrow, mobilized peripheral blood, and umbilical cord blood represent the major sources of transplantable HSCs, but their availability for use is limited by both compatibility between donor and recipient and required quantity. Although increasing evidence suggests that somatic HSCs can be expanded to meet current needs, their in vivo potential is concomitantly compromised after ex vivo culture. In contrast, human embryonic stem cells (hESC) possess indefinite proliferative capacity in vitro and have been shown to differentiate into the hematopoietic cell fate, giving rise to erythroid, myeloid, and lymphoid lineages using a variety of differentiation procedures.
but the true promise of stem cells is directed differentiation. applications that come to mind include organ replication, neurogenesis and treatment of neurodegenerative afflictions, mimicking the natural differentiation process of stem cells to regenerate cells perfectly matched to a patient. this isnt quite possible with erythropoietics. while a good start, they aren't the most promising horizon. after all, if we perfect messing with totipotents, we can generate multipotent erythropoietic cells for some applications to solve the tumor issue.
how differentiated are umbilical stem cells? are they totipotent like embryonics? or are they erythropoietic stem cells since they are from cord blood? obviously, the best solution to all of this is research in de-differentiation of eryhtropoietic stem cells into totipotent cells.
You will ALWAYS find mixtures of decent, honest people in a much outweighed ratio with lying, backstabbing, climb-my-way-to-the-top types. It just so happens, for the most part, the scientific community (as well as the world) became flooded with the latter.
wow, someone's been taking their pessimism supplements. let's have some proof. as far as i'm concerned, the bad eggs are few and far between. for every example of your latter population of backstabbers, i'm sure you can name 10 decent, hard-working people. i know i can. in science too. wouldnt be such an interesting story if they were reporting "hey this biologist passaged some cells correctly"
In regards to your free-market approach towards people and employment, I think it is a flawed assumption. I may have some bias, being a scientist (and biologist) myself, so take everything I say with an appropriate sized grain of salt.
That said, I believe that science is one of many professions where you must have motivation beyond money and personal advancement to make a career. Going the route of a PhD in any field is not a walk in the park, nor is it the most financially rewarding route. I can't count the number of times I could've taken a sweet computer programming position in industry and been extremely comfortable in life compared to my current starving student existence as a doctoral candidate. But I could never imagine myself in any field other than science and being able to goto work daily with as clear a moral conscience and purpose in life as I have now.
The system of peer review in place reviewing government funded grants is much more developed than the collusory and corrupt system you picture. The study sections that are responsible for reviewing NIH grant applications are diverse and their composition varies annually. There is no small council of elite scientists that has the final say on all government funded grants in science. That being said, there is influence of politics within the field (personal rivalries etc), but those sorts of biases are not easy to translate into denying funding. There must always be valid scientific analysis supporting any grant's funding decision. The influence of politics is heavy at the top (ie- the overall NIH budget), but as far as individual grants, the influence of traditional partisan politics is not direct. That decision is solely left to the scientists.
The selection process for career scientists, at least in the US, begins far before you get to this stage of your career. Peer review and criticism of your rigorousness as a scientist is constantly evaluated beginning for all career scientists as they enter grad school, and often even in undergraduate education. You undergo the scrutiny of a multitude of people who impact your career's development, many if not most of whom have strong ideological views on science and protect the field by upholding high standards for a scientist's motivations. The survival approach to the career is most often unsuccessful and results in a student either dropping out or being failed out.
I guess in the end, I'm just trying to say that the picture is extremely complicated, and that the scientific community has put many precautions into place to uphold the integrity of individuals in the field. The scandal surrounding Prof Hwang is disappointing, but hardly representative of the state of the field as a whole. And lets not overlook the fact that it takes a talented and dedicated individual to fabricate scientific data.
As for the official word on the scandal:
"Hwang admitted on 16 December that there were errors in the 2005 stem-cell paper, but denied fraud. He maintains that 11 patient-specific stem-cell lines were created as reported, but six were never frozen, and subsequently became contaminated. He says five lines being thawed now will prove his success."
Nature 438, 1056-1057 (22 December 2005)
Let's just wait and see what happens with that.
Slashdot Mirror
enzyme activity isn't completely binary.
If a patient stays on a regimen until only latent cells are left, we can then use a latent-specific immune cell activator to purge these last remaining infected cells. However, the latter part of this treatment methodology has yet to be discovered; until it is, yes the patient must remain on the drugs for as long as possible.
The drugs in the cocktail would not create selective pressure for alternate receptors since they all act on aspects of the virus life cycle downstream of the receptor/entry point.
The HIV virus does not "embed" itself into the dna of a victim.
Lesson on the viral life cycle:
HIV --> injects RNA genome + tRNA primer --> reverse transcription to double stranded DNA --> integration ("embedding") into host genome --> transcription of viral genes from integrated HIV DNA to spliced and unspliced mRNA--> translation/export of mRNA and formation of virus particles
It inserts it's rna into t-cells and uses the t-cells to replicate itself. The problem is that this kills the t-cells, thus killing you.
The cause of massive T cell loss in HIV infection has yet to be concretely determined. Direct cell killing due to viral cytopathic effect is not believed to be a major factor. Rather the dysregulation of immune activation, function and apoptosis associated with infection are thought to be the primary causes for T cell loss. Your death is also not a direct effect of T cell loss, but rather the emergence of a combination of opportunistic infections and oncogenic viruses such as Kaposi's Sarcoma Herpesvirus which kills a person.
It does NOT hide away and wait to pop out the second a victim stops taking his or her cocktail.
And actually, the latent reservoir DOES wait to pop out the second a victim stops taking his/her cocktail. It isn't quite as malicious as you imply though...the "popping out" occurs naturally as cells from the resting memory reservoir are activated by antigen stimulus and then reinitiate productive infection. This occurs periodically even when a patient is on medications, but fail to produce virus due to drug blocking virus life cycle. But when a patient has to inevitably stop treatment due to prohibitive cost, toxicity or other side effects, these re-activation events are allowed to proceed and reinitiate full-blown infection.
It cannot attack neurons. Only t-cells.
It has been shown that HIV can enter neurons, but it just fails to produce virus. HIV infects not only T cells, but macrophages as well. Additionally, some groups have reported evolution of viruses which can use their co-receptors as the entry point, opening HIV to a wider range of host cells.
Sorry about this double post, low sleep = mistakes. But I wanted the full and proper reply to go up.
Using highly active anti-retroviral treatment (HAART) regimens comprised of a combination of 3-4 drugs from the following classes: protease inhibitors, non-nucleoside reverse transcriptase inhibitors, nucleoside reverse transcriptase inhibitors, we can essentially eliminate all productively infected cells and the only infected cells remaining are transcriptionally latent, producing no new virus, causing no symptoms and giving the patient essentially virus-free blood. There are a number of suspected "reservoir" populations where latently infected cells can be found (resting memory CD4 T cells, macrophages). Only latently infected memory T cells have been proven to be clinically relevant. The stats on infection for these cells are that on average around 1 in every 10^6 resting memory CD4 T cells is latently infected in any given patient. This number can vary between HAART patients from less than 1 in 10^6 to even 10s in 10^6. In order for HIV to replicate, it must integrate itself into the host cell's DNA in every infected cell. Only a select few cells will integrate, then become latent and enter hibernation. Eliminating these cells will not likely cause any perceptible deficit in immune function.
HIV infects cells of the immune system; HIV's receptor is CD4, coreceptors are CXCR4 and CCR5, all found exclusively on immune cells, not neurons. The cell death and dementia associated with HIV is most likely a bystander effect, where immune cells in the brain are replicating virus and some product or downstream effect of the replication cycle is causing neighboring cells to die. Again though, the number of infected cells is low. The main issue with the brain is that it is immune privileged, so it is under less rigorous immune surveillance than the rest of the body. Combine that fact with the fact that HIV infects immune cells and disrupts their function, and you have a recipe for disaster in the brain. Antiretrovirals that can penetrate the BBB can effectively stop virus replication there without destroying nervous function.
Using highly active anti-retroviral treatment (HAART) regimens comprised of a combination of 3-4 drugs from the following classes: protease inhibitors, non-nucleoside reverse transcriptase inhibitors, nucleoside reverse transcriptase inhibitors, we can essentially eliminate all productively infected cells and the only infected cells remaining are transcriptionally latent, producing no new virus, causing no symptoms and giving the patient essentially virus-free blood. There are a number of suspected "reservoir" populations where latently infected cells can be found (resting memory CD4 T cells, macrophages). Only latently infected memory T cells have been proven to be clinically relevant. The stats on infection for these cells are that on average around 1 in every 10^6 resting memory CD4 T cells is latently infected in any given patient. This number can vary between HAART patients to
HIV infects cells of the immune system; HIV's receptor is CD4, coreceptors are CXCR4 and CCR5, all found exclusively on immune cells, not neurons. The cell death and dementia associated with HIV is most likely a bystander effect, where immune cells in the brain are replicating virus and some product or downstream effect of the replication cycle is causing neighboring cells to die. Again though, the number of infected cells is low. The main issue with the brain is that it is immune privileged, so it is under less rigorous immune surveillance than the rest of the body. Combine that fact with the fact that HIV infects immune cells and disrupts their function, and you have a recipe for disaster in the brain. Antiretrovirals that can penetrate the BBB can effectively stop virus replication there without destroying nervous function.
Never say never. I think there are a number of studies that have yet to be done on latently infected cells with integrated HIV. Without fully characterizing the latent cells, we can't really say that there isn't something different about them that can't be exploited for targeting treatments.
If leaders of the field are to be believed, anti-retroviral drug regimens can currently eliminate all infected cells in the body save for these latently infected ones. And if developments arise that allow specific targeting and elimination of the latent cells, boom problem is solved. I'm prophesizing a system of targeted immune activation to draw out the hiding infected cells, and letting existing drugs get rid of em.
I think the problem of replication and infection in the brain is also poorly understood. Personally, I think the extravasation of infected immune cells into the brain is the source of replication, rather than any of the resident cells. The cells in the brain that can host replication are extremely limited (microglia, barely in astrocytes), and there are already promising developments to stop replication with drugs that easily cross the blood brain barrier (minocycline stops hiv replication in microglia, attenuates neuronal apoptosis).
Gene therapy to deliver RNAi targeting HIV mRNAs offers another potential solution to this whole problem. I think the tools and most of the knowledge are out there. We just need to develop them to the point of usability. However, I really have little faith in the utility of the drug outlined in this study. Tons of crap kills HIV in a test tube. Let's see how toxic this drug is and its bioavailability/pharmocokinetic profile.
dont forget NOS and related species that it pumps out. also enormously important in signaling of the brain.
I see a huge loophole in this thinking. Free radicals and reactive oxygen species, while bad in excess, are involved in numerous signaling pathways of the body and are enormously important in phenomena like immune activation. Massive supplementing of anti-oxidants may address the suspected negative role of oxidative stress in shortening telomeres , but raises tons of others. If you dose yourself with anti-oxidants and screw up the normal thresholds for oxidant-related signaling, who knows what myriad of negative effects may arise?
Jeez o flip people, read the blasted article. They want to identify pathways involved in pressure sensing, not just to determine cause of death. This has implications in general biology and is hardly mindless killing of rodents. Now I'm not saying that this couldn't have been done without sacrifice of the animal, but I would imagine it would be quite hard to get a good mRNA profile of a cell under transient mechnical pressure. Really, how the hell would you do that?
As for all you broadly anti-animal testing people...I can only say that as an SIV monkey researcher myself, really the best and only truly valuable way to study pathophysiology of mant diseases is with an animal model. Really anything in cell culture is much less useful considering how things change when you scale up into an animal with multiple organ systems. Sad but true. So some monkeys/mice/dogs/cats/guinea pigs/ferrets/flies/sea urchins/etc gotta go. I really want to see more sea urchins on PETA shirts though. That would make my day.
My one major grip is that in the article they really needed to better control the position of the cells analyzed to the site of insult. What would've been cool is if they had seen a graident effect of gene expression, highest in cells near d=0 (site of strangulation/string contact) and tapering as you examined cells farther away in the neck. This would also provide more evidence on the theory of mechanosensing since as you move away from d=0, the mechanical force on the cells decreases. The 4 genes found upregulated only really has one solid link to the cytoskeleton and gives evidence of a compression-sensitive signaling pathway. Ikematsu I., et al. Legal Medicine article in press, (2006)
My 2c.
i think priority needs to go into embryonic, toti-potent cells so that we can understand the process of differentiation completely, and then we will know exactly where we stand with the potential cell fates of other types of stem cells we have less controversial access to (cord blood stem cells, adult bone marrow etc) and can actually make them therapeutically viable with cell culture methods ex vivo.
starting major therapeutic research with hematopoietic stem cells seems alot to me like starting to build a building by stacking premade floors instead of hiring an architect and engineer. Experimental Hematology, 2005 Sep;33(9):987-96.
but the true promise of stem cells is directed differentiation. applications that come to mind include organ replication, neurogenesis and treatment of neurodegenerative afflictions, mimicking the natural differentiation process of stem cells to regenerate cells perfectly matched to a patient. this isnt quite possible with erythropoietics. while a good start, they aren't the most promising horizon. after all, if we perfect messing with totipotents, we can generate multipotent erythropoietic cells for some applications to solve the tumor issue.
how differentiated are umbilical stem cells? are they totipotent like embryonics? or are they erythropoietic stem cells since they are from cord blood? obviously, the best solution to all of this is research in de-differentiation of eryhtropoietic stem cells into totipotent cells.
In regards to your free-market approach towards people and employment, I think it is a flawed assumption. I may have some bias, being a scientist (and biologist) myself, so take everything I say with an appropriate sized grain of salt. That said, I believe that science is one of many professions where you must have motivation beyond money and personal advancement to make a career. Going the route of a PhD in any field is not a walk in the park, nor is it the most financially rewarding route. I can't count the number of times I could've taken a sweet computer programming position in industry and been extremely comfortable in life compared to my current starving student existence as a doctoral candidate. But I could never imagine myself in any field other than science and being able to goto work daily with as clear a moral conscience and purpose in life as I have now. The system of peer review in place reviewing government funded grants is much more developed than the collusory and corrupt system you picture. The study sections that are responsible for reviewing NIH grant applications are diverse and their composition varies annually. There is no small council of elite scientists that has the final say on all government funded grants in science. That being said, there is influence of politics within the field (personal rivalries etc), but those sorts of biases are not easy to translate into denying funding. There must always be valid scientific analysis supporting any grant's funding decision. The influence of politics is heavy at the top (ie- the overall NIH budget), but as far as individual grants, the influence of traditional partisan politics is not direct. That decision is solely left to the scientists. The selection process for career scientists, at least in the US, begins far before you get to this stage of your career. Peer review and criticism of your rigorousness as a scientist is constantly evaluated beginning for all career scientists as they enter grad school, and often even in undergraduate education. You undergo the scrutiny of a multitude of people who impact your career's development, many if not most of whom have strong ideological views on science and protect the field by upholding high standards for a scientist's motivations. The survival approach to the career is most often unsuccessful and results in a student either dropping out or being failed out. I guess in the end, I'm just trying to say that the picture is extremely complicated, and that the scientific community has put many precautions into place to uphold the integrity of individuals in the field. The scandal surrounding Prof Hwang is disappointing, but hardly representative of the state of the field as a whole. And lets not overlook the fact that it takes a talented and dedicated individual to fabricate scientific data. As for the official word on the scandal: "Hwang admitted on 16 December that there were errors in the 2005 stem-cell paper, but denied fraud. He maintains that 11 patient-specific stem-cell lines were created as reported, but six were never frozen, and subsequently became contaminated. He says five lines being thawed now will prove his success." Nature 438, 1056-1057 (22 December 2005) Let's just wait and see what happens with that.