Tuesday, November 25, 2014

SCCmec IX- Mec C gene

Greetings

One of the most common known microbe of interest to the public and scientists equally is MRSA. It has been so deeply engraved in to the medical literature that it needs no introduction. If you are connected to medical microbiology you would know that, MRSA is a genetic output of a gene called MecA gene, sitting inside a gene cassette called Sccmec element. But many probably don't know there are variants, the most well known is called MecC which also manifests as MRSA phenotype, but doesn't lend itself to easy identification in the clinical laboratory.

Table 1: Mec gene variants. 
A strain called S. aureus isolate, LGA251, was first isolated in study of bovine population which showed phenotypic resistance to cefoxitin but latex agglutination PBR2a and MecA- PCR negative, despite repeated tests. On sequencing, a novel gene which was just 69% genetically similar to MecA was identified. The new variant was referred as MecA-LGA251. Subsequently reports emerged on the presence of this strain from multiple regions and retrospective sample search identified from a Danish blood, 1975. As per the current consensus, the MecC lies in a novel cassette XI SCCmec. The first question is why not MecB? MecB is identified in Macrococcus caseolyticus as a variant from MecA. See Table 1 for list of variants known.

There is no clear evidence on origins of MecC gene. The gene has been isolated from Staphylococcus stepanovicii, Staphylcoccus scirui and a variant tentatively called MecC1 isolated from SCCmec IX-like element in Staphylococcus xylosus.

The MecC gene (Also called as Class C) contains MecA and truncated MecR1 due to insertion of a IS431 upstream of MecA, and hyper-variable region and IS431 downstream of MecA. Based on the symmetry of insertion, two distinct class C mec gene complexes are recognized. Class C1 Mec gene complex, the IS431 upstream of MecA has the same orientation as the IS431 downstream of MecA, while in the class C2 Mec gene complex, the orientation of IS431 upstream of MecA is reversed. C1 and C2 are considered to have probably evolved independently. IS431 is a member of staphylococcal insertion sequence-like element and is constantly associated with Methicillin resistance.

Fig 1: Oxacillin/ Cefoxitin sensitivity in
MecA vs MecC types.
In a study by Torok etal; of 62 MecC MRSA isolates 88.7% were susceptible to oxacillin but resistant to cefoxitin (S/R), 11.3% were resistant to both oxacillin and cefoxitin (R/R), and none were susceptible to both antimicrobials. Based on the finding it was projected that Oxacillin Susceptible/ Cefoxitin resistant profile probably represents a MecC MRSA. Considering the current data, with an expected MecC S aureus is less than 4%, the positive predictive value of identification based on antibiotic disc screening is very low (less than 50%). Hence the current recommendation is testing for Mec gene using universal Mec primers which can pick multiple Mec gene variants.

Methicillin resistance is now an old and almost a universal phenomenon in S aureus. The arrival of new varieties represents new challenges in terms of diagnostics. This blog post is just a primer to keep you thinking, how many more flavors of Mec could be out there.

ResearchBlogging.org
García-Álvarez, L etal. Meticillin-resistant Staphylococcus aureus with a novel mecA homologue in human and bovine populations in the UK and Denmark: a descriptive study The Lancet Infectious Diseases, 11 (8), 595-603 DOI:10.1016/S1473-3099(11)70126-8

Ito T, Hiramatsu K, Tomasz A, de Lencastre H, Perreten V, Holden MT, Coleman DC, Goering R, Giffard PM, Skov RL, Zhang K, Westh H, O'Brien F, Tenover FC, Oliveira DC, Boyle-Vavra S, Laurent F, Kearns AM, Kreiswirth B, Ko KS, Grundmann H, Sollid JE, John JF Jr, Daum R, Soderquist B, Buist G, & International Working Group on the Classification of Staphylococcal Cassette Chromosome Elements (IWG-SCC) (2012). Guidelines for reporting novel mecA gene homologues. Antimicrobial agents and chemotherapy, 56 (10), 4997-9 PMID: 22869575

Cartwright EJ, Paterson GK, Raven KE, Harrison EM, Gouliouris T, Kearns A, Pichon B, Edwards G, Skov RL, Larsen AR, Holmes MA, Parkhill J, Peacock SJ, & Török ME (2013). Use of Vitek 2 antimicrobial susceptibility profile to identify mecC in methicillin-resistant Staphylococcus aureus. Journal of clinical microbiology, 51 (8), 2732-4 PMID: 23720794

Paterson GK, Harrison EM, & Holmes MA (2014). The emergence of mecC methicillin-resistant Staphylococcus aureus. Trends in microbiology, 22 (1), 42-7 PMID: 24331435

Wednesday, November 19, 2014

Indian Ebola survivor- Quarantined.

Greetings


    Seldom have I got the chance to talk about any topic again and again in this blog that has only attracted more readers. Oh yes, You got it right. Once again, talking about Ebola 2014. When the outbreak began, it wasn't predicted by any that this would be such a mega outbreak. As of on November 11, 2014 a total of 14,383 Ebola cases have been reported as of November 11 from three West African countries (Source). The media attention that has been received is simply great. And when a country announces they have a fresh case, its the fastest news in circulation.

    The most important news, Democratic Republic of Congo has been declared officially as "outbreak free", after not registering any new case since October 4. There are no new cases for 42 days which is the officially accepted time to declare as outbreak free. Of course the after effects are still being dealt with. And the second most, India quarantines a Ebola survivor. I have purposefully mentioned as a "survivor" and not as the first case in India. There seems to be a lot of panic in the media reports and the story has been blended in press as of to indicate India has its case. Hmmm. Let me try and tease that situation out.

    The suspect is a 26-year-old survivor, successfully treated for Ebola in Liberia and released from a health facility back in late September. He had no symptoms. He was cleared to fly after he had tested negative by standard blood tests (In fact he tested 3 times as negative). However, his semen tested positive. This discussion seems to be over to me after listening to multiple episodes of TWiV podcasts in recent shows, were this has been discussed in immense details. The basic point boils down to the fact that Ebola seems to be surviving in patients semen (Culture positive) even after they have recovered from illness for about 2- 3 months, possibly more. To the best of knowledge, there are no documented case of sexually transmitted case of Ebola. I have though seen arguments over the internet, that it could be possible and there is a documented evidence of similar scenario in a related virus- "Marburg virus". Best advice at this point is no sex after Ebola recovery for at least 90 days. There is a definitive lack of research on the possibilities of Ebola latency in body fluids.

      I totally agree with the move of health officials quarantine for the "just in case" scenario.  However, It should be considered that he has been treated, survived and cleared by blood tests. This indicates that he is no more diseased. However, to call it the first case is unwarranted. In fact technically speaking, he is not even a case. The outbreak currently seems to be currently in a decline phase and the outbreak should be officially over worldwide, hopefully in a few months.

ResearchBlogging.org
Bausch DG, Towner JS, Dowell SF, Kaducu F, Lukwiya M, Sanchez A, Nichol ST, Ksiazek TG, & Rollin PE (2007). Assessment of the risk of Ebola virus transmission from bodily fluids and fomites. The Journal of infectious diseases, 196 Suppl 2 PMID: 17940942

Friday, November 14, 2014

Microbiome- Follow up post

Greetings

  In my previous post, I talked about the growing field of microbiome and tried to put important concepts of virome in a snapshot pattern. I realized that I should have cited more examples and some concentrated a bit more on microbiome, to get the reader a full picture. So, this post is a follow up for my previous post.

First, let me revisit the debated question of microbiome. "Is it worth to call our microbiome a yet another organ"? This is a well discussed question with science thinkers and practitioners taking both sides of opinion and there is no consensus. However more and more of the scientific community is beginning to accept the yes part of it. The point that the microbiome is more than significantly associated with multiple physiological components is striking enough to be called as an organ. Gnotobiotic rats are maintained in such artificial conditions, shows that natural life without microbiome is probably impossible. That argument delivered, let us at least tentatively agree it as another organ (But unlike other organs, in terms of dynamic nature).

I'm pretty sure you have heard at least one example similar to the following. Two identical persons with similar exposure to environmental factors (Let's say mosquito bite), and one of them keeps getting infection. Th other appears resistant always. The earliest of the arguments was "Genetics". With more research pouring in this seems to be possible even if the genetics was much similar (Say in siblings) and genetics may not account, nor chance. Such questions have led researchers to question if there is more to it. A set of gene similarity don't mean much these days, since concepts such as epigenetics has to be considered for variability. But microbiome probably produces a gene pool that can account for a million more variation to be considered, and that is why the the hypothesis of "microbiome influence" is damn attractive.

Not convinced yet? In addition to the previous post citing articles (I have previously posted multiple blogs on the same concept, Indeed this blog site is full of such examples), here I will present a couple of examples that stress on what I have said.

Perhaps the most compelling of the evidence is microbiome influence on weight. Obesity is considered as a disease in the current era and there is enough genetic factors that lie around the whole concept. However, off late evidence has begun to accumulate that microbe gene pool is also important. Studies have been conducted on humanized mice to show that microbiome can have a significant impact on obesity. It has been demonstrated that by transferring the microbiome, from gut obesity can be influenced. Lean mice can be made obese and other way around. More recently deep sequencing from human gut has shown supportive results.

In a recent example I cited, C difficile has got an important rival C scindens, which can reduce the C diff effect (Read my previous post here). This is not the only such study. For example Ruminococcus obeum is shown to significantly effect the virulence of V cholerae. This is mediated through a inter species quorum sensing, specifically R obeum AI-2 which repress V cholerae virulence genes. There are more such examples in literature, and more on coming. You just need to look.

There are more examples. For example, microbial composition is shown to influence how frequently you will get a mosquito bite. Skin flora metabolites are the cause of odor, signatures of which can be detected by the mosquito, It has been shown that a particular pattern of microbiota composition is more attractive to mosquito. Another one, bacterial colonization in the wound is common concurrence. The type of composition has been shown to impact the healing capabilities in terms of time and quality.

The first question that has been often raised is why can't we get such data for every condition? Is it reliable. I have already discussed the dynamic nature and the technical challenge in evaluating the flora composition in previous post. Additionally understanding the pathways between every microbial entity is currently out of the technical capabilities. Working with more than a million connections is simply a challenge.

More recently the whole concept of microbiome has met with a challenge of addressing contamination. In a article published in nature, there is a lot of discussion on issue of contaminating sequences, based on papers published in BMC biology and PloS One. The point basically boils down to the fact that the reagents used in two commonly used sequencing techniques -16S rRNA and whole-genome shotgun metagenomics, contain contaminating sequences. The lack of negative control sequence has impacted the way we look into the deep sequencing technique. The point is illustrated in the statement by Walker, "We haven’t challenged anyone directly. We hope the message will stand for itself. We’re trying to nip it in the bud now before it becomes more of an issue.” Source

So what are the implications?

One of the microbiota based therapy is projected to be Fecal transplantation (FTM). The success story of treating C diff infection, by FTM has led many people to argue that probably "microbiota transfer", can be the answer to many of the conditions. In other words, there is a tendency to designate "Good" & "Bad" microbiome. My projection was that, if we can recolonize with "Good microbiota", for other conditions such as asthma, where it can be influential, that would be great. Of course we don't know at this point what is that combination in any of our normal flora system. However, A post in ASM blog (Link), has led me to rethink this. Probably, just like genes its not good or bad. Its the context that matters.

Story has just begun to uncover, and am sure I will be revisiting these concepts. 

ResearchBlogging.org
Baquero, F., & Nombela, C. (2012). The microbiome as a human organ Clinical Microbiology and Infection, 18, 2-4 DOI:10.1111/j.1469-0691.2012.03916.x

Ridaura VK, Faith JJ, Rey FE, Cheng J, Duncan AE, Kau AL, Griffin NW, Lombard V, Henrissat B, Bain JR, Muehlbauer MJ, Ilkayeva O, Semenkovich CF, Funai K, Hayashi DK, Lyle BJ, Martini MC, Ursell LK, Clemente JC, Van Treuren W, Walters WA, Knight R, Newgard CB, Heath AC, & Gordon JI (2013). Gut microbiota from twins discordant for obesity modulate metabolism in mice. Science, 341 (6150) PMID:24009397

Hsiao A, Ahmed AM, Subramanian S, Griffin NW, Drewry LL, Petri WA, Haque R, Ahmed T, & Gordon JI (2014). Members of the human gut microbiota involved in recovery from Vibrio cholerae infection. Nature PMID: 25231861

Saturday, November 08, 2014

Microbiome- Dwelling a little deep

Greetings

      Everyone is familiar with the nomenclature "Normal flora". They represent a set of microbes that inhabit us. Estimates have claimed that there are nearly 10 times more microbes in human body than the cells. Debates exist as to if this is true or an exaggeration. But it is irrelevant at this point. It is for sure however that they interact and influence our cellular machinery. Their influence is studied in terms of Immunological signatures, neurobiology, oncogenesis etc. Most of the textbooks don't acknowledge this yet, since the details are just beginning to emerge. I have blogged about these aspects a variety of time in this blog which you could check out.

Fig 1: A representation of common members
of bacteriome. Source

   I have been thinking for sometime, "Is it worth to call our microbiome a yet another organ"?. I haven't posed this question for the first time. This question has been discussed in great depth in a variety of conferences, academic papers etc. What is not realized is the human microbiome is much more than that, and its dynamic is too difficult to study. The term microbiome in itself is considered as a sloppy definition (Read ASM blog post here). For the purpose of clarity, let us stick to the definition that microbiome denote all microbes at a site. The concept of microbiome is derived from the development of deep sequencing methods with billions of reads. Even the best of microbial culture method cannot retrieve and analyse every possible species in a site. Clearly we had to await the emergence of modern technology. A massive Human microbiome project, is currently pursuing studies to understand the human microbiome. It is clear that microbiome is a signature of individual and there is a huge variation. Its uniqueness is so striking that it has been proposed as a forensic tool. Body sites presumed to be sterile in healthy humans, such as the vascular endothelium, Brain etc have been shown to be colonized without apparent signs of disease. Such publications have shaken the ground beliefs of sterile sites in body.

     Till extremely recently the word microbiome was almost exclusively studies on bacteriome. This is because, almost all bacteria have a signature identifiable sequence in one single gene- 16S ribosomal sequence. Amplify and identify all the 16S deep sequences (not as simple as said), a metagenomic approach and boom you have everything. Fungal microbiome is a little more harder and the virome is the hardest. As represented in Fig 2, expected virome content is much more than bacteriome or mycobiome. For virome, you just deep sequence everything you find and remove the known bacteriala nd other DNA matches. The rest is matched directly with known database and similar looking viral genomes from database. Often there will be "grey sequences" (casually referred as dark matter) which doesn't match with anything. 

Fig 2: A rough representation of
microbiome content.
     So much of information to bring you into a question, one of the readers had asked me after reading my previous post on "Algal virus and cognition". Is there examples of good or bad effects of human virome? And suddenly I realized that I have never talked much about the Human Virome. 

    As can be understood from above, "microbiome" is a massive subject of interest with too much grey area to even speculate on its functionality. As I have said, bacteria has been studied more in connection with a variety of conditions. But it simply seems logical to me, to extend that where there is a bacteria, viruses will tag along. But the current virome literature is in its infancy and so I chose to put up some examples taken from studies. This should help in getting the answer across allowing room for exploring.

Box 1: Projected contents of
human virome.
   For every bacterial species known, there are bacteriophages. Gut microbiome is perhaps the most heavily colonized microbiome. with more than 35000 varieties of bacteria in the site, I expect at least a million (if not billion) phages there. The best part is they form a defense layer. Innate immunity acquired via such phages are referred as, phage-mediated immunity (PMI). Study by Barr etal, had shown that our mucus membrane is heavily colonized by lytic phages, which tend to attack incoming invaders and serve as first line of defense. Due to their extreme importance in defense, there is a expected evolutionary pressure to retain these phages. It is not known as to how these phages are maintained, or if at all it is maintained by the host or the gut microbiota. As the next story will show bacteria can equip themselves with more than toxins to counter other invading pathogen. They can arm themselves with phages against others. So maybe, the microbiome maintains the phages. After all its the requirement of normal flora to stay in competition for their own benefit.

     Let me digress a little bit, to cite maintenance of virus as an armory. This is based on an article published by Lora Hooper and team. The study showed that Enterococcus faecalis has in its genome integrated genomes of two different phage elements (one gives structure to the composite, while the other helps it infect victims), which can be unleashed on demand. These phages attacks other bacteria providing a competing advantage. This strain is called V583. That's a proof of concept, and maybe PMI is replenished through similar mechanism. I however, have no data to support my idea.

     I have talked about HERV in a post almost about 2 years ago emphasizing the fact that our very existence as to humans owes a lot to these viral pieces. Just to remind, the placental formation is based on a viral protein (Syncytium beta)- HERV-W envelope glycoprotein coding gene. Read my previous post here. Many more such marvels are slowly being discovered. As explained in a previous post (Link), Inactively residing herpes in neurons may have beneficial effects.

     Just as the bacteriome influences outcome in many different conditions so does viruses. Studies are currently studying viral composition in a variety of disease conditions. One of the most cited study is by Moya etal; showed there is less viral diversity in the Crohn’s disease patients compared to healthy. Additionally they found these where mostly Retroviridae members in effected patients. My take on this there is a lack of phage varieties that effect the bacteriome. It is known that there is a significant importance of bacteriome quality and type in crohn's disease.

    The said field offers new research avenues, but comes with its own set of challenges. Microbiomes are not stagnant types in a person. At least some percentage of it vary continuously. By using a CRISPR based tagging approach, in a 11 months study it was shown that the virome can vary by anywhere between 25 and 75% between every sample. This means that it is computationally and logically difficult to characterize a virome and associate it with a condition.

   Just to add to flavor there is a realm of fungus in the microbiome. Recently published data suggests that fungus too have dynamic interaction. A study has gone as far as to characterize how fungal microbiome can dictate T cell balances (which can be done by bacteria and some helminths as well), thereby creating a risk for allergies. And then there are phages of fungus called as mycophages which am sure will be present as a part of our virome. The entire field of mycophages is currently a dark region, so forget about commenting on its effects.

  To conclude, I will say microbiome is currently a hot topic. Connection has been made with a variety of conditions and microbiome. But proving and characterizing every connection is very hard at least with current technology. Virome is a step next to it, though science will make its advance slowly.

ResearchBlogging.org
Lax S, Smith DP, Hampton-Marcell J, Owens SM, Handley KM, Scott NM, Gibbons SM, Larsen P, Shogan BD, Weiss S, Metcalf JL, Ursell LK, Vázquez-Baeza Y, Van Treuren W, Hasan NA, Gibson MK, Colwell R, Dantas G, Knight R, & Gilbert JA (2014). Longitudinal analysis of microbial interaction between humans and the indoor environment. Science, 345 (6200), 1048-52 PMID:25170151

Costello EK, Lauber CL, Hamady M, Fierer N, Gordon JI, & Knight R (2009). Bacterial community variation in human body habitats across space and time. Science, 326 (5960), 1694-7 PMID:19892944

Wylie KM, Weinstock GM, & Storch GA (2012). Emerging view of the human virome. Translational research : The journal of laboratory and clinical medicine, 160 (4), 283-90 PMID:22683423

Barr JJ, Youle M, & Rohwer F (2013). Innate and acquired bacteriophage-mediated immunity. Bacteriophage, 3 (3) PMID: 24228227

Pérez-Brocal V, García-López R, Vázquez-Castellanos JF, Nos P, Beltrán B, Latorre A, & Moya A (2013). Study of the viral and microbial communities associated with Crohn's disease: a metagenomic approach. Clinical and translational gastroenterology, 4 PMID: 23760301

Kim YG, Udayanga KG, Totsuka N, Weinberg JB, Núñez G, & Shibuya A (2014). Gut dysbiosis promotes M2 macrophage polarization and allergic airway inflammation via fungi-induced PGE₂. Cell host & microbe, 15 (1), 95-102 PMID: 24439901

Friday, November 07, 2014

Algal virus and Cognition- Is there a link?

Greetings

    One of the most important accepted rule in the world of pathogens is the specificity of host. This rule is especially true when it comes to viruses. Most of the viral pathogens have a very restricted range of host. With drastic mutations, the virus maybe able to infect other hosts which are closely related to the original host. But, if I will cite an example of algal virus probably sitting in human throat, that would blow your mind of. And if I add to it that it may possibly influence your neurological activity, you will probably think I have gone nuts. I was equally mesmerized when I heard of the study and headlines in internet saying "Algal virus impacts cognition". I decided to look into a little more detail.

     The virus under discussion here is ATCV-1 (Acanthocystis turfacea chlorella virus 1), a member of Chlorovirus. ACTV-1 has been previously reported to be found in human oral sample metagenomic analysis, in psychiatric patients though it was never formally tested for its importance. Being a virus of algae, it can be easily thought of as a contaminant since they are found in water reservoirs. Previous literature has evidence for detection of the viral signatures in brain biopsy samples. However, its validity couldn't be convincingly established.

Box 1: Highlights of the study.
     In this new study, the researcher's studied normal and psychiatric patients for the presence of viral signatures in the oral flora. The study was able to show that of those infected with the virus, performed 10% worse than uninfected people on standard cognitive tests. So the most important question that arises from the result is does it mean anything? This was further tested by using a mouse model. The results looks quite compelling. Other than a significant difference in cognitive tests between infected and non infected, changes in roughly 1300 genes were also shown in hippocampus. By using modern bioinformatics analysis, the genes effected were found to be involved in pathways related to dopamine receptor signaling, cyclin-dependent kinase 5 (CDK5) signaling, antigen presentation, immune cell adhesion, and eukaryotic initiation factor 2. Note that dopamine is a central component of many psychiatric conditions.

   Chloroviruses are common in inland waters throughout the world, usually in high numbers. Is the virus actively involved or is it through some non specific mechanism such as inflammation that has caused these changes. The current suggestion is. most possibly through a non specific inflammatory reaction. I had also like to take some more opinions into consideration. First, the virus was given to mice along with its host algae. Did that create an effect? Second, is it possible that the presence of ACTV-1 predisposes to some phenomenon (mostly inflammation), which accelerates the effect by some other compound. Or perhaps, does the antibodies produced against the virus induce any cross effect, such as is the case with PANDAS where culprit is Group A streptococcus.

    The current paper however, does warrant the need to look into more details. In my opinion, the study is novel and has a point. However, 10% effect and no compelling mechanism is asking for more data and studies. Its too early to claim "Algal virus impacts cognition". Remember, Association is not causation.

ResearchBlogging.org
Yolken RH, Jones-Brando L, Dunigan DD, Kannan G, Dickerson F, Severance E, Sabunciyan S, Talbot CC Jr, Prandovszky E, Gurnon JR, Agarkova IV, Leister F, Gressitt KL, Chen O, Deuber B, Ma F, Pletnikov MV, & Van Etten JL (2014). Chlorovirus ATCV-1 is part of the human oropharyngeal virome and is associated with changes in cognitive functions in humans and mice. PNAS PMID: 25349393

Wednesday, November 05, 2014

Ebola-2014: Still in news

Greetings

   In less than a couple of months, Ebola has become the search term of interest and is currently the most focused component of concern. And rightly so. It has been accused by many that there are no readily approved treatment or vaccines against this infection. But it is to be understood that scientists don't work like magic. Science needs its own time to make discoveries. But then scientists are working out of their way to bring in promising results.

    The current outbreak is perplexing, given its unprecedented geographical distribution and number of cases involved. As per the estimates the total number of reported cases is more than 13500 and deaths nearing 5000. Liberia alone has 6,500 cases and 2,413 deaths reported as of Oct. 31. And then there will be a set of unreported cases. Models have estimated a very high number of total cases which includes reported and unreported cases. However, its debatable if the models are over estimating the current prevalence and incidence.

     Other than the Zmapp, and a couple of experimental drugs (Link) which in itself is under testing phase, there is not much available in the hands to counter the current outbreak. This provides the most attractive time to come up with anything novel. As I have previously discussed in this blog vaccine is perhaps the best candidate (Link). However, only a vector vaccine containing replication competent VSV (Vesicular stomatitis virus) carrying Ebola Glycoprotein has shown to be of some use. The other well explored area is use of adenovirus carrying antigens as a vaccine. In a recently published hot paper- this has been used in the form of nasal spray, promising to provide long-term immunity.

    This isn't actually a new discovery. Literature has been published on this by Maria Croyle and team in 2006 (Link), showing that nasal delivery of Adenovirus Expressing the Ebola Glycoprotein conferred protection in a mice model. The vaccine basically consists of human adenovirus serotype 5 (AdHu5) expressing the wild-type ZEBOV glycoprotein sequence from a CMV promoter. This combination is called Ad-CMVZGP. The new study by Croyle and team showed that the vaccine elicited good immune response, through Intra nasal route in comparison with other routes. The protection was demonstrated 21 weeks after immunization.

   The study offers great advantages, as one of the author in study says "The main advantage of our vaccine platform over the others in clinical testing is the long-lasting protection after a single intranasal dose. This is important since the longevity of other vaccines for Ebola that are currently being evaluated is not fully understood. Moreover, the nasal spray immunization method is more attractive than a needle vaccine given the costs associated with syringe distribution and safety." Source

   Another vaccine that has promising pre clinical data ChAd-Ebola; Chimpanzee-Adenovirus chAD3-ZEBOV. The Phase I trial is expected to be initiated at the earliest and results will be available by early 2015.

The current outbreak has exposed the unpreparedness to counter the Ebola. As I always say, basic biology needs to be done. But, then there is a great support to come up with defense mechanism that may help us be prepared at least the next time. And the question of prospects of the vaccine, only the next set of data will tell.

ResearchBlogging.org
Croyle, M., Feldmann, H., Jones, S., Wilson, J., & Kobinger, G. (2006). 595. Nasal Delivery of Adenovirus Expressing the Ebola Glycoprotein Protects Mice Against Ebola Virus in the Presence of Preexisting Immunity to the Vaccine Carrier. Molecular Therapy, 13 DOI: 10.1016/j.ymthe.2006.08.669

Richardson JS, Yao MK, Tran KN, Croyle MA, Strong JE, Feldmann H, & Kobinger GP (2009). Enhanced protection against Ebola virus mediated by an improved adenovirus-based vaccine. PloS one, 4 (4) PMID: 19390586

Choi, J., Jonsson-Schmunk, K., Qiu, X., Shedlock, D., Strong, J., Xu, J., Michie, K., Audet, J., Fernando, L., Myers, M., Weiner, D., Bajrovic, I., Tran, L., Wong, G., Bello, A., Kobinger, G., Schafer, S., & Croyle, M. (2014). A Single Dose Respiratory Recombinant Adenovirus-Based Vaccine Provides Long-Term Protection for Non-Human Primates from Lethal Ebola Infection. Molecular Pharmaceutics DOI: 10.1021/mp500646d